Apoptosis is a spontaneous programmed cell death process,which is closely related to the occurrence and development of tumors.Inducing apoptosis of tumor cells has become an important way of anti-tumor therapy.Studies...Apoptosis is a spontaneous programmed cell death process,which is closely related to the occurrence and development of tumors.Inducing apoptosis of tumor cells has become an important way of anti-tumor therapy.Studies have found that clearing heat-toxin Chinese medicine has a significant effect on inducing apoptosis,which may be the key mechanism of anti-tumor of Chinese medicine.By reviewing the theoretical origin of anti-tumor TCM of clearing heat-toxin Chinese herbs and the pharmacological research progress of intervening apoptosis-related proteins to promote apoptosis of tumor cells,this paper provides a basis for TCM to induce apoptosis of tumor cells to prevent and treat malignant tumors.展开更多
This work conducted a four-week metabolism test on rats to study the digestion and absorption characteristics of five protein-based krill products prepared from Antarctic krill as raw material.It aimed to provide theo...This work conducted a four-week metabolism test on rats to study the digestion and absorption characteristics of five protein-based krill products prepared from Antarctic krill as raw material.It aimed to provide theoretical support for the effective use of Antarctic krill protein and the development of novel protein resources.The results showed that the weight gain and true digestibility of the rats fed with krill meat,surimi and ordinary krill powder were significantly higher(P<0.05)than those of the rats fed with traditional casein.Compared to casein,proteins from the five Antarctic krill products were found to significantly improve the net protein utilization(P<0.05),and reduce the total cholesterol and triglycerides in the serum of rats(P<0.05).In summary,the Antarctic krill protein-based products with high nutritional values can be used as a potential novel protein resource in the food industry.展开更多
BACKGROUND:This study aims to explore whether Xuebijing(XBJ) can improve intestinal microcirculation dysfunction in sepsis and its mechanism.METHODS:A rat model of sepsis was established by cecal ligation and puncture...BACKGROUND:This study aims to explore whether Xuebijing(XBJ) can improve intestinal microcirculation dysfunction in sepsis and its mechanism.METHODS:A rat model of sepsis was established by cecal ligation and puncture(CLP).A total of 30 male SD rats were divided into four groups:sham group,CLP group,XBJ + axitinib group,and XBJ group.XBJ was intraperitoneally injected 2 h before CLP.Hemodynamic data(blood pressure and heart rate) were recorded.The intestinal microcirculation data of the rats were analyzed via microcirculation imaging.Enzyme-linked immunosorbent assay(ELISA) kits were used to detect the serum levels of interleukin-6(IL-6),C-reactive protein(CRP),and tumor necrosis factor-α(TNF-α) in the rats.Histological analysis and transmission electron microscopy were used to analyze the injury of small intestinal microvascular endothelial cells and small intestinal mucosa in rats.The expression of vascular endothelial growth factor A(VEGF-A),phosphoinositide 3-kinase(PI3K),phosphorylated PI3K(p-PI3K),protein kinase B(Akt),and phosphorylated Akt(p-Akt) in the small intestine was analyzed via Western blotting.RESULTS:XBJ improved intestinal microcirculation dysfunction in septic rats,alleviated the injury of small intestinal microvascular endothelial cells and small intestinal mucosa,and reduced the systemic inflammatory response.Moreover,XBJ upregulated the expression of VEGF-A,p-PI3K/total PI3K,and p-Akt/total Akt in the rat small intestine.CONCLUSION:XBJ may improve intestinal microcirculation dysfunction in septic rats possibly through the VEGF-A/PI3K/Akt signaling pathway.展开更多
AIM To investigate the effect of Boschniakiarossica(BR)extract on expression of GST-P,p53 and p21<sup>ras</sup>proteins in early stage of chemicalhepatocarcinogenesis in rats and its anti-inflammatory ac...AIM To investigate the effect of Boschniakiarossica(BR)extract on expression of GST-P,p53 and p21<sup>ras</sup>proteins in early stage of chemicalhepatocarcinogenesis in rats and its anti-inflammatory activities.METHODS The expression of tumor marker-placental form glutathione S-transferase(GST-P),p53 and p21<sup>ras</sup>proteins were investigated byimmunohistochemical techniques and ABCmethod.Anti-inflammatory activities of BR werestudied by xylene and croton oil-induced mouseear edema,carrageenin,histamine and hotscald-induced rat pow edema,adjuvant-inducedrat arthritis and cotton pellet-induced mousegranuloma formation methods.RESULTS The 500 mg/kg of BR-H<sub>2</sub>O extractfractionated from BR-Methanol extract hadinhibitory effect on the formation of DEN-inducedGST-P-positive foci in rat liver(GST-P stainingwas 78% positive in DEN+AAF group vs 20%positive in DEN+AAF+BR group,P【0.05)andthe expression of mutant p53 and p21<sup>ras</sup>proteinwas lower than that of hepatic preneoplasticlesions(33% and 22% positive respectively inDEN+AAF group vs negative in DEN+AAF+BRgroup).Both CH<sub>2</sub>Cl<sub>2</sub> and H<sub>2</sub>O extracts from BRhad anti-inflamatory effect in xylene and crotonoil-induced mouse ear edema(inhibitory rateswere 26%-29% and 35%-59%,respectively). BR-H<sub>2</sub>O extract exhibited inhibitory effect incarrageenin,histamine and hot scald-inducedhind paw edema and adjuvant-induced arthritis inrats and cotton pellet-induced granulomaformation in mice.CONCLUSION BR extract exhibited inhibitory effect on formation of preneoplastic hepatic foci in early stage of rat chemical hepato-carcinogenesis. Both CH<sub>2</sub>CI<sub>2</sub> and H<sub>2</sub>O extracts from BR exerted anti-inflammatory effect in rats and mice.展开更多
AIM To .investigate if sleep deprivation is able to increase the expression of inducible heat shock protein 70 in gastric mucosa and its possible role in mucosal defense.METHODS Rats for sleep disruption were placed i...AIM To .investigate if sleep deprivation is able to increase the expression of inducible heat shock protein 70 in gastric mucosa and its possible role in mucosal defense.METHODS Rats for sleep disruption were placed inside a computerized rotating drum, gastric mucosa was taken from rats with 1, 3 and 7 d sleep deprivation. RT-PCR,immunohistochemistry and Western blotting were used to determine the expression of heat shock protein 70.Ethanol (500 mL@ L 1, I.g.) was used to induce gastric muceea damage.RESULTS RT-PCR, Western blotting and immunostaining confirmed that the sleep deprivation as a stress resulted in significantly greater expression of inducible heat shock protein 70 in gastric mucosa of rats. After the 500mL@ L-1 ethanol challenge, the ulcer area found in the rats with 7 d sleep deprivation (19.15 ± 4.2) mm2 was significantly lower (P<0.01) than the corresponding control (53.7 ± 8.1) mm2.CONCLUSION Sleep deprivation as a stress, in addition to lowering the gastric mucosal barrier, is able to stimulate the expression of inducible heat shock protein 70 in gastric mucosa of rats, the heat shock protein 70 may play an important role in gastric mucosal protection.展开更多
AIM:To assess the expression of nestin and glial fibrillary acidic protein(GFAP)in rat retina after optic nerve transection.METHODS:Rats were randomly divided into normal control group,sham group and operation gro...AIM:To assess the expression of nestin and glial fibrillary acidic protein(GFAP)in rat retina after optic nerve transection.METHODS:Rats were randomly divided into normal control group,sham group and operation group,and used for establishing an animal model of optic nerve transection.Retinal specimen of each group was collected at 3,48h,7and 14d postoperative.Nestin and GFAP expressions on sagittal sections were analyzed by immunohistochemical staining,and protein extraction was analyzed by Western blot.RESULTS:Immunohistochemical analysis showed that nestin positive staining was rarely detected in normal control group and sham group,while sham group showed weak positive staining at 3h postoperative,the reaction gradually increased at 48h postoperative,and reached its maximum at 7d postoperative,and then decreased at 14d postoperative.Compared to the expression of GFAP,there was not statistically significant obvious difference among three groups(P〉0.05).Result of Western blot method was consistent with that of immunohistochemical method.CONCLUSION:The expression of nestin increased in a time dependent fashion in Müller cells of retina following optic nerve transection,which was statistically significant,but there was no obvious difference in GFAP expression.The results indicate that an increase in colloid synthesis in retina following optic nerve transection can improve the retinal neurons’environment.展开更多
Objective: To study the synthesis of heat shock pro- tein 70 (HSP70) by zinc ( ZnSO_4) and its protective effect during cold preservation in rat liver by estab- lishment of a simple cold preservation model. Methods: W...Objective: To study the synthesis of heat shock pro- tein 70 (HSP70) by zinc ( ZnSO_4) and its protective effect during cold preservation in rat liver by estab- lishment of a simple cold preservation model. Methods: Wistar rats were divided into 5 groups (n =6): control group untreated before operation; Zn- 1, Zn-2, and Zn-3 groups treated before operation with zinc sulfate (Zn^(2+) 5 mg/kg, 10 mg/kg, 15 mg/ kg respectively); H group treated with heat shock (42.5 ℃×15 min). The livers of the rats were pre- served in UW solution for 6, 12, 24 hours. The re- sults of heat shock protein (HSP) synthesis were ana- lyzed with Western blot. The aspartate aminotrans- ferase (AST) and lactic dehydrogenase (LDH) values of perfusion and histological findings were evaluated. Results: A great amount of HSPs was synthesized af- ter pretreatment with zinc and heat shock. The AST and LDH values of the Zn-1, Zn-2 and H groups were significantly lower than those of the C group (P <0.05). But the value of the Zn-3 group was much higher. Histologically, mild injury was observed in the Zn-1, Zn-2 and H groups, but severe injury in the Zn-3 group. Conclusions: Zn^(2+), as a potent and feasible inducer of HSP expression, is able to protect the liver for cold preservation. Proper induction dosage of Zn^(2+) ranges from 5 mg/kg to 10 mg/kg, and Zn^(2+) 15 mg/ kg could not be a stress conditioning factor for its ad- verse effect on rat liver.展开更多
Objective To investigate the impact of sub-chronic Aluminium-maltolate [Al(mal)s] exposure on the catabolism of amyloid precursor protein (APP) in rats. Methods Forty adult male Sprague-Dawley (SD) rats were ran...Objective To investigate the impact of sub-chronic Aluminium-maltolate [Al(mal)s] exposure on the catabolism of amyloid precursor protein (APP) in rats. Methods Forty adult male Sprague-Dawley (SD) rats were randomly divided into five groups: the control group, the maltolate group (7.56 mg/kg BW), and the Al(mal)s groups (0.27, 0.54, and 1.08 mg/kg BW, respectively). Control rats were administered with 0.9% normal saline through intraperitoneal (i.p.) injection. Maltolate and Al(mal)s were administered to the rats also through i.p. injections. Administration was conducted daily for two months. Rat neural behavior was examined using open field tests (OFT). And the protein expressions and their mRNAs transcription related with APP catabolism were studied using enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (RT-PCR). Results The expressions of APP, 13-site APP cleaving enzyme 1 (BACEI) and presenilin-1 (PSi) proteins and their mRNAs transcription increased gradually with the increase of Al(mal)3 doses (P〈0.05). The enzyme activity of BACEI in the 0.54 and 1.08 mg/kg Al(mal)s groups increased significantly (P〈0.05). The expression of 8-amyloid protein (AS) 1-40 gradually decreased while the protein expression of A81-42 increased gradually with the increase of Al(mal)s doses (P〈0.05). Conclusion Result from our study suggested that one of the possible mechanisms that Al(mal)s can cause neurotoxicity is that Al(mal)s can increase the generation of A81-42 by facilitating the expressions of APP, β-, and γ-secretase.展开更多
Objective:To investigate the expression of Runx3 and TGF-β<sub>1</sub> protein in the colon from rats with irritable bowel syndrome(IBS).Methods:Rat model for IBS was established by intracolonic instill...Objective:To investigate the expression of Runx3 and TGF-β<sub>1</sub> protein in the colon from rats with irritable bowel syndrome(IBS).Methods:Rat model for IBS was established by intracolonic instillation with acetic acid and restraint stress methods,which was confirmed by determinating the visceral sensitivity of the animals,including abdominal withdrawal reflex (AWR) score and the electronic behavior of the abdomen wall.The rats were randomly assigned into three groups:IBS,group(restraint stress,n=25);IBS<sub>2</sub> group(both instillation with acetic acid and restraint stress,n=25) and Control group(n=16).The colonic tissue samples were collected for histological study and the expression of Runx3 and TGF-β<sub>1</sub> proteins were detected by immunohistochemistry.Meanwhile,the relationship of these two proteins was calculated. Results:Visceral hypersensitivity(AWR and abdominal electrical activity) was significantly enhanced in IBS,and IBS<sub>2</sub> groups than other groups.The colon tissue in all groups did not show any signs of inflammation.Furthermore,the expression of Runx3 and TGF-β<sub>1</sub> protein in the colon from all groups show no significant difference(P】0.05),with no remarkable relevancy between each other(P】0.05).Conclusions:The rat model for IBS was successfully established. We did not find any significant changes in the expression of Runx3 and TGF-β<sub>1</sub> protein in the colon tissue from IBS rats,suggesting that the quantitative changes may be not the way by which Runx3 and TGF-β<sub>1</sub> protein play their roles in IBS.The accurate roles of Runx3 and TGF-β<sub>1</sub> proteins in the pathogenesis of IBS remains to be further studied.展开更多
Previous studies have suggested that glutathione-S-transferase π (GST-π) over-expression in the brain tissue is associated with refractory epilepsy. However, whether the change in GST-π level in the peripheral bl...Previous studies have suggested that glutathione-S-transferase π (GST-π) over-expression in the brain tissue is associated with refractory epilepsy. However, whether the change in GST-π level in the peripheral blood is in line with that in brain tissue remains unknown. This study examined the correlation between GST-π in brain tissue and that in peripheral blood in rat models of pilocarpine-induced refractory epilepsy. The animals were divided into drug-resistant group and drug-responsive group according to the response to anti-epileptic drugs. GST-π expression in brain tissue was immunohistochemically determined, while the expression of GST-π in peripheral blood was analyzed by Western blotting. In the hippocampus and cortex, GST-π was mainly found in the cytoplasm and membrane of neurons, and the GST-π expression level was higher in drug-resistant group than in the drug-responsive group and saline control group (P〈0.05). Moreover, there was no significant difference between responders and saline control animals (P〉0.05). The change in expression of GST-π in peripheral blood showed the same pattern as that in brain tissues, suggesting GST-π might contribute to drug resistance in epilepsy. Importantly, the GST-π over-expression in peripheral blood could be used as a marker for resistance to anti-epileptic agents.展开更多
Objective :To elucidate whether cell multiplication, apoptosis, glucose intake and p-Akt protein expression of bone Mesenchyreal Stem Cells(MSCs) of rats is influenced by a hypoxic environment ex vivo. Methods :Pa...Objective :To elucidate whether cell multiplication, apoptosis, glucose intake and p-Akt protein expression of bone Mesenchyreal Stem Cells(MSCs) of rats is influenced by a hypoxic environment ex vivo. Methods :Passage 3 of bone marrow MSCs taken from Wistar rats,were cultured in a culturing chamber with 94%N2,1%O2,5%CO2 at 37℃. At different hypoxia time points ,0,0.5, 1,4 and 8 h, glucose uptake was assayed by using radiation isotope ^3H-G, Apoptotic Rate(AR) and dead rate(DR) were analyzed by flow cytometry(FCM) after Annexin V/PI staining, cell multiplication(by MTr methods) and p-Akt protein by immunocytochemistry and western blot. Results :Assay for CD29^± ,CD44^± ,CD71^± ,CD34^-, Tn T^±(after 5-azacytidine agent inducing) and ALP^±(after bone differentiation agent inducing) suggested these bone-derived cells were MSCs. The ^3H-G intaking ratio (CPM/ flask value:157 ± 11,110 ± 11,107 ± 13,103 ± 10,100 ± 9 and 98 ± 10) of MSCs at different hypoxia time points, significantly decreased compared to that of normoxia(P 〈 0.01) and tended to descend slowly with hypoxia time duration, for which there was no statistical significance(P 〉 0.05). The AR(0.09 ± 2.03%,12.9 ± 1.72%,13.7 ± 2.26%,13.8 ± 3.01%,14.1 ± 2.78% and 14.7 ± 4.01% at 0,0.5,1,4 and 8 h,respectively,P 〈 0.01) and DR (0.04, ± 1.79% ,0.93 ± 1.85% ,3.11 ± 2.14% ,4.09 ± 2.36% ,4.72 ± 2.05% and 4.91 ± 3.72% at 0,0.5,1,4 and 8 h, respectively, P 〈 0.05) at different hypoxia time points significantly increased compared to those time in normoxia; The AR further went up with time (P 〈 0.05), however there was no statistical significance (P 〉 0.05) for the DR. Optical absorption value of MTr methods at different hypoxia time points significantly decreased compared to those with a corresponding normoxia time (P 〈 0.01) and degraded with time (in an hypoxic environment -P 〈 0.01). IOD of p-Akt protein of MSCs at different hypoxia time points significantly increased (0.367 ± 0.031,0.556 ± 0.023,0.579 ± 0.013, 0.660 ± 0.024, 0.685 ± 0.039 and 0.685 ± 0.011, respectively) compared to their equivalents in normoxia (P〈0.05), however, there was no statistical significance (P 〉 0.05) for different hypoxia time points. Hypoxia may result in ultramicrostructure changes, such as defluvium of Microvilli, apoptotic body, "margination" and so on and are further aggravated with hypoxia time stretching. Conclusion: Hypoxia may lead to a depression of MSCs intaldng glucose, creep of cell multiplication, upregulation of p-Akt protein and apoptosis of MSCs ex vivo.展开更多
This study aimed to explore the pathological change to hippocampal neurons and the expression of growth associated protein 43 in 21-day-old young rats following chronic intermittent hypoxia. Hematoxylin-eosin staining...This study aimed to explore the pathological change to hippocampal neurons and the expression of growth associated protein 43 in 21-day-old young rats following chronic intermittent hypoxia. Hematoxylin-eosin staining results showed varying degrees of degeneration and necrosis in hippocampal neurons depending on the modeling time. Immunohistochemistry revealed that growth associated protein 43 expression in young rats following chronic intermittent hypoxia decreased, but that levels were still higher than those of normal rats at each time point, especially 4 weeks after modeling. During 1 5 weeks after modeling, a slow growth in rat weight was observed. Experimental findings indicate that chronic intermittent hypoxia may induce growth dysfunction and necrosis of hippocampal neurons, as well as increase the expression of growth associated protein 43 in young rats.展开更多
BACKGROUND Intestinal inflammation is a common digestive tract disease, which is usually treated with hormone medicines. Hormone medicines are effective to some extent, but long-term use of them may bring about many c...BACKGROUND Intestinal inflammation is a common digestive tract disease, which is usually treated with hormone medicines. Hormone medicines are effective to some extent, but long-term use of them may bring about many complications.AIM To explore the protective effects of panax notoginseng saponin(PNS) against dextran sulfate sodium(DSS)-induced intestinal inflammatory injury through phosphoinositide-3-kinase protein kinase B(PI3K/AKT) signaling pathway inhibition in rats.METHODS Colitis rat models were generated via DSS induction, and rats were divided into control(no modeling), DSS, DSS + PNS 50 mg/k, and DSS + PNS 100 mg/kg groups. Then, the intestinal injury, oxidative stress parameters, inflammatory indices, tight junction proteins, apoptosis, macrophage polarization, and TLR4/AKT signaling pathway in colon tissues from rats in each of the groups were detected. The PI3 K/AKT signaling pathway in the colon tissue of rats was blocked using the PI3K/AKT signaling pathway inhibitor, LY294002.RESULTS Compared with rats in the control group, rats in the DSS group showed significantly shortened colon lengths, and significantly increased disease activity indices, oxidative stress reactions and inflammatory indices, as well as significantly decreased expression of tight junction-associated proteins. In addition, the DSS group showed significantly increased apoptotic cell numbers,and showed significantly increased M1 macrophages in spleen and colon tissues.They also showed significantly decreased M2 macrophages in colon tissues, as well as activation of the PI3K/AKT signaling pathway(all P < 0.05). Compared with rats in the DSS group, rats in the DSS + PNS group showed significantly lengthened colon lengths, decreased disease activity indices, and significantly alleviated oxidative stress reactions and inflammatory responses. In addition, this group showed significantly increased expression of tight junction-associated proteins, significantly decreased apoptotic cell numbers, and significantly decreased M1 macrophages in spleen and colon tissues. This group further showed significantly increased M2 macrophages in colon tissues, and significantly suppressed activation of the PI3K/AKT signaling pathway, as well as a dose dependency(all P < 0.05). When the PI3K/AKT signaling pathway was inhibited, the apoptosis rate of colon tissue cells in the DSS + LY294002 group was significantly lower than that of the DSS group(P < 0.05).CONCLUSION PNS can protect rats against DSS-induced intestinal inflammatory injury by inhibiting the PI3K/AKT signaling pathway, and therefore may be potentially used in the future as a drug for colitis.展开更多
Previous studies have reported that non-human primates and rodents exposed to lead during brain development may become dependent on the deposition of pre-determined β-amyloid protein (Aβ),and exhibit upregulation ...Previous studies have reported that non-human primates and rodents exposed to lead during brain development may become dependent on the deposition of pre-determined β-amyloid protein (Aβ),and exhibit upregulation of β-site amyloid precursor protein expression in old age.However,further evidence is required to elucidate the precise relationship and molecular mechanisms underlying the effects of early lead exposure on excessive Aβ production in adult mammals.The present study investigated the effects of lead exposure on expression of β-amyloid precursor protein cleavage enzyme-1 (BACE-1) in the rat retina and the production of Aβ in early development,using the retina as a window for studying Alzheimer's disease.Adult rats were intraocularly injected with different doses of lead acetate (10μmol/L,100μmol/L,1 mmol/L,10 mmol/L and 100 mmol/L).The results revealed that retinal lead concentration,BACE-1 and its cleavage products β-C-terminal fragment and retina Aβ1-40 were all significantly increased in almost all of the lead exposure groups 48 hours later in a dose-dependent manner.The only exception was the 10μmol/L group.The distribution of BACE-1 in the retina did not exhibit obvious changes,and no distinctive increase in the activation of retinal microglia was apparent.Similarly,retinal synaptophysin expression did not exhibit any clear changes.These data suggest that lead exposure can result in the upregulation of retinal neuron BACE-1 expression in the early period of development and further increase the overproduction of Aβ1-40 in the retina.Our results provided novel insight into the molecular mechanisms underlying environmentally-induced Alzheimer's disease.展开更多
All motions provide sensory, motoric, and reflexive input to the central nervous system, as well as playing an important role in cerebral functional plasticity and compensation. Cerebral plasticity has become the theo...All motions provide sensory, motoric, and reflexive input to the central nervous system, as well as playing an important role in cerebral functional plasticity and compensation. Cerebral plasticity has become the theoretical basis of neurorehabilitation. Studies of cerebrovascular disease, in particular, demonstrate that regeneration is accompanied by multiple forms of plasticity, such as functional and structural, in different phases of stroke rehabilitation. This study was designed to measure synaptic plasticity and expression of associated proteins to analyze the effect of rehabilitation training on learning and memory in a rat model of cerebral infarction. Results suggest that rehabilitation training increases expression of nerve growth factor associated protein 43, brain-derived neurotrophic factor, and neural cell adhesion molecules, and also promotes cerebral functional plasticity.展开更多
A previous study from our group showed that Jiawei Wendan decoction inhibits protein expression of interleukin-1β, 2, and 6, as well as plasma neuropeptide Y, P substance and somatostatin in the hippocampus of depres...A previous study from our group showed that Jiawei Wendan decoction inhibits protein expression of interleukin-1β, 2, and 6, as well as plasma neuropeptide Y, P substance and somatostatin in the hippocampus of depression rat models. The present study analyzed the influence of Jiawei Wendan decoction on the mitogen-activated protein kinase signal transduction pathway in the hippocampus. Results demonstrated that Jiawei Wendan decoction effectively upregulated expression of small molecular G proteins, extracellular regulated kinase 1/2, and activated ribosomal S6 kinase protein in the rat hippocampus. In addition, Jiawei Wendan decoction exhibits antidepressant effects similar to fluoxetine. The underlying mechanisms were shown to be dependent on increased mitogen-activated protein kinase signal transduction pathway activity.展开更多
Objective To study whether there is the apoptosis of neural cells and the expression of Bcl-2 protein in intracerebral hemorrhage (ICH) in model of rats, for the further understanding the mechanism of the delayed dama...Objective To study whether there is the apoptosis of neural cells and the expression of Bcl-2 protein in intracerebral hemorrhage (ICH) in model of rats, for the further understanding the mechanism of the delayed damage of the neural cells around the hematoma after ICH. Methods Fifty SD rats were randomly divided into 5 groups, ten in each. With the Group A as the control, the rest 40 were used to set up intracerebral hemorrhage model. The brains were taken out at 12 th , 24 th , 48 th and 72 th hours, respectively. Apoptosis cells were detected with terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL), and the expression of Bcl-2 protein was detected with immunochemical stainging methed (SP). Results In the control group, no apoptosis cells and Bc1-2 protein were detected. In rest groups, the apoptosis cells and Bc1-2 protein were expressed in different degree. Apoptosis rates verified and corresponded with the time after ICH, with the peak at 48 th -72 th hour after hemorrhage. The peak rate of apoptosis cells was (24.50±2.69)% and Bcl-2 protein expression was (20.76±1.97)% . There was significant difference between the experimental groups and control (P<0.05), and no linear relationship between the apoptosis rate and the expression of Bcl-2 protein. Conclusion Apoptosis may be an important factor in the secondary trauma of ICH. There is a time leg after hemorrhage. All this is instructive to clinical treatment in time. Bcl-2 protein keeps increasing in a certain time after hemorrhage, but not synchronize with the cell apoptosis. This indicates that bcl-2 has the effect to reduce the apoptosis of neural cells.展开更多
Emerging evidence has suggested global histone H4 acetylation status plays an important role in neural plasticity. For instance, the imbalance of this epigenetic marker has been hypothesized as a key factor for the de...Emerging evidence has suggested global histone H4 acetylation status plays an important role in neural plasticity. For instance, the imbalance of this epigenetic marker has been hypothesized as a key factor for the development and progression of several neurological diseases. Likewise, astrocytic reactivity-a wellknown process that markedly influences the tissue remodeling after a central nervous system injury-is crucial for tissue remodeling after spinal cord injury(SCI). However, the linkage between the above-mentioned mechanisms after SCI remains poorly understood. We sought to investigate the relation between both glial fibrillary acidic protein(GFAP) and S100 calcium-binding protein B(S100B)(astrocytic reactivity classical markers) and global histone H4 acetylation levels. Sixty-one male Wistar rats(aged ~3 months) were divided into the following groups: sham; 6 hours post-SCI; 24 hours post-SCI; 48 hours post-SCI; 72 hours post-SCI; and 7 days post-SCI. The results suggested that GFAP, but not S100B was associated with global histone H4 acetylation levels. Moreover, global histone H4 acetylation levels exhibited a complex pattern after SCI, encompassing at least three clearly defined phases(first phase: no changes in the 6, 24 and 48 hours post-SCI groups; second phase: increased levels in the 72 hours post-SCI group; and a third phase: return to levels similar to control in the 7 days post-SCI group). Overall, these findings suggest global H4 acetylation levels exhibit distinct patterns of expression during the first week post-SCI, which may be associated with GFAP levels in the perilesional tissue. Current data encourage studies using H4 acetylation as a possible biomarker for tissue remodeling after spinal cord injury.展开更多
BACKGROUND: High incidence of stroke at interchange period of autumn and winter was demonstrated by epidemiological survey, and the specific causes should be further investigated. OBJECTIVE: To investigate the influ...BACKGROUND: High incidence of stroke at interchange period of autumn and winter was demonstrated by epidemiological survey, and the specific causes should be further investigated. OBJECTIVE: To investigate the influence of artificial cold exposure on the incidence of stroke in renovascular hypertensive rats (RHR), and analyze the association with blood pressure and cold-inducible RNA binding protein (CIRP) mRNA expression in brain tissue. DESIGN: A completely randomized grouping design, a randomized control animal trial. SETTINGS: Lab of Neurology, the First Affiliated Hospital of Sun Yat-sen University; Department of Chemistry, Open laboratory of Chemical Biology, Institute of Molecular Technology for Drug Discovery and Synthesis, University of Hong Kong. MATERIALS: Male SD rats (n=460), weighing 80 - 100 g were obtained from Guangdong Province Health Animal Unit. A modified RXZ-300A intelligent artificial climate cabinet (Ningbo Jiangnan Instrument Co. ,Ltd., China). METHODS: The experiment were processed in the Lab of Neurology, the First Affiliated Hospital of Sun Yat-sen University and the Open Laboratory of Chemical Biology, Institute of Molecular Technology for Drug Discovery and Synthesis, University of Hong Kong from October 2004 to November 2005. Rats (n = 400) were operated to establish 2-kidney 2-clip RHR model as described previously. The sham-operated rats (n =60) served as normotensive controls. Eight weeks later, 300 of RHR were randomly selected according to their systolic blood pressure (SBP) and divided into 3 sub-groups (n =100 per group): mild hypertensive group (SBP of 160 - 200 mm Hg), moderate hypertensive group (SBP of 200 - 220 mm Hg) and severe hypertensive group (SBP 〉 220 mm Hg). Each group was further divided into two groups (n =50) under ACE and non-ACE. Normal sham-operated SD rats (n =60), SBP 〈 140 mm Hg, were randomly divided into two groups: Sham-operated control group (n =30) under ACE and non-ACE. To establish the ACE and non-ACE treatment, rats were housed individually in artificial climate cabinet, and ACE was designed as three cycles of 12-hour light of 22℃ (7 : 00 - 19 : 00) and 12-hour dark of 4℃(19 : 00 - 7 : 00). The non-ACE group was kept at 22℃ throughout the experiment. MAIN OUTCOME MEASURES: Blood Pressure changes were measured and stroke symptom were observed; Expression of the CIRP were examined by reverse transcription-polymerase chain reaction. RESULTS: Finally 360 rats were involved in the analysis of results. ①Incidence of stroke: The incidence of stroke in 2k2c RHR was significantly higher after a three-day intermittent (12-hour) ACE (29.3%) as compared with that in non-ACE (17.3%) (P 〈 0.05). Furthermore, the severe hypertensive 2k2c RHR (BP 〉 220 mm Hg) was found to have much higher incidence of stroke (66%, 33/50) than the mild (8%, 4/50) and moderate (18%) hypertensive 2k2c RHR. ②CIRP mRNA in brain tissue: ACE treatment stimulated the mRNA expression of CIRP in non-stroke 2k2c RHR but not in stroke 2k2c RHR (P 〈 0.05). CONCLUSION: High blood pressure and low expression of CIRP are associated with ACE induced stroke.展开更多
Approximately 40-50 β-defensins are predominantly expressed in the male reproductive system of mammals. This selective expression raises the question as to the roles of these molecules in innate immunity and fertilit...Approximately 40-50 β-defensins are predominantly expressed in the male reproductive system of mammals. This selective expression raises the question as to the roles of these molecules in innate immunity and fertility in the male reproductive tract. Rat β-defensin 22 is an epididymis-specific β-defensin expressed in segments 12-14 of the epididymis. This protein contains both β-defensin and lectin signature sequences, yet its antimicrobial activity and carbohydrate-binding ability have not been shown. We herein demonstrated the antimicrobial activity of recombinant rat β-defensin 22 against Escherichia coliand Candida albicans. Its lectinJike activity was also investigated by demonstrating its binding ability with heparin beads. This heparin-binding activity implies some potential roles for this defensin in determining the fertilisation capabilities of sperm.展开更多
基金Research Project of Jing'an District,Shanghai,No.2019QN09Shanghai Youth Science and Technology Talents Sailing Program,No.20YF1449900The Third Jing'an District Modern Chinese Medicine Teacher Training Project(ZYSC-2022-8)。
文摘Apoptosis is a spontaneous programmed cell death process,which is closely related to the occurrence and development of tumors.Inducing apoptosis of tumor cells has become an important way of anti-tumor therapy.Studies have found that clearing heat-toxin Chinese medicine has a significant effect on inducing apoptosis,which may be the key mechanism of anti-tumor of Chinese medicine.By reviewing the theoretical origin of anti-tumor TCM of clearing heat-toxin Chinese herbs and the pharmacological research progress of intervening apoptosis-related proteins to promote apoptosis of tumor cells,this paper provides a basis for TCM to induce apoptosis of tumor cells to prevent and treat malignant tumors.
基金financially supported by the Marine S&T Fund of Shandong Province for Pilot National Laboratory for Marine Science and Technology(Qingdao)(No.2022 QNLM030002)the National Key R&D Program of China‘Formation Mechanism of Antarctic Krill Fishery and Key Technologies for Efficient Utilization of Resources’:Antarctic Krill High Value Product Creation and Industrialization Demonstration(No.2018YFC1406806)the Technology Innovation Project of Qingdao Marine Science and Technology Pilot National Laboratory,Shandong Provincial Marine Science,the Technology Fund Major‘Dark Blue Fishery’4-2:Construction of Antarctic Krill Processing Technology Process System(No.2018SDKJ0304-2)。
文摘This work conducted a four-week metabolism test on rats to study the digestion and absorption characteristics of five protein-based krill products prepared from Antarctic krill as raw material.It aimed to provide theoretical support for the effective use of Antarctic krill protein and the development of novel protein resources.The results showed that the weight gain and true digestibility of the rats fed with krill meat,surimi and ordinary krill powder were significantly higher(P<0.05)than those of the rats fed with traditional casein.Compared to casein,proteins from the five Antarctic krill products were found to significantly improve the net protein utilization(P<0.05),and reduce the total cholesterol and triglycerides in the serum of rats(P<0.05).In summary,the Antarctic krill protein-based products with high nutritional values can be used as a potential novel protein resource in the food industry.
基金supported by a grant from National Natural Science Foundation of China (82272196)。
文摘BACKGROUND:This study aims to explore whether Xuebijing(XBJ) can improve intestinal microcirculation dysfunction in sepsis and its mechanism.METHODS:A rat model of sepsis was established by cecal ligation and puncture(CLP).A total of 30 male SD rats were divided into four groups:sham group,CLP group,XBJ + axitinib group,and XBJ group.XBJ was intraperitoneally injected 2 h before CLP.Hemodynamic data(blood pressure and heart rate) were recorded.The intestinal microcirculation data of the rats were analyzed via microcirculation imaging.Enzyme-linked immunosorbent assay(ELISA) kits were used to detect the serum levels of interleukin-6(IL-6),C-reactive protein(CRP),and tumor necrosis factor-α(TNF-α) in the rats.Histological analysis and transmission electron microscopy were used to analyze the injury of small intestinal microvascular endothelial cells and small intestinal mucosa in rats.The expression of vascular endothelial growth factor A(VEGF-A),phosphoinositide 3-kinase(PI3K),phosphorylated PI3K(p-PI3K),protein kinase B(Akt),and phosphorylated Akt(p-Akt) in the small intestine was analyzed via Western blotting.RESULTS:XBJ improved intestinal microcirculation dysfunction in septic rats,alleviated the injury of small intestinal microvascular endothelial cells and small intestinal mucosa,and reduced the systemic inflammatory response.Moreover,XBJ upregulated the expression of VEGF-A,p-PI3K/total PI3K,and p-Akt/total Akt in the rat small intestine.CONCLUSION:XBJ may improve intestinal microcirculation dysfunction in septic rats possibly through the VEGF-A/PI3K/Akt signaling pathway.
基金the National Natural Science Foundation of China,No.39660021
文摘AIM To investigate the effect of Boschniakiarossica(BR)extract on expression of GST-P,p53 and p21<sup>ras</sup>proteins in early stage of chemicalhepatocarcinogenesis in rats and its anti-inflammatory activities.METHODS The expression of tumor marker-placental form glutathione S-transferase(GST-P),p53 and p21<sup>ras</sup>proteins were investigated byimmunohistochemical techniques and ABCmethod.Anti-inflammatory activities of BR werestudied by xylene and croton oil-induced mouseear edema,carrageenin,histamine and hotscald-induced rat pow edema,adjuvant-inducedrat arthritis and cotton pellet-induced mousegranuloma formation methods.RESULTS The 500 mg/kg of BR-H<sub>2</sub>O extractfractionated from BR-Methanol extract hadinhibitory effect on the formation of DEN-inducedGST-P-positive foci in rat liver(GST-P stainingwas 78% positive in DEN+AAF group vs 20%positive in DEN+AAF+BR group,P【0.05)andthe expression of mutant p53 and p21<sup>ras</sup>proteinwas lower than that of hepatic preneoplasticlesions(33% and 22% positive respectively inDEN+AAF group vs negative in DEN+AAF+BRgroup).Both CH<sub>2</sub>Cl<sub>2</sub> and H<sub>2</sub>O extracts from BRhad anti-inflamatory effect in xylene and crotonoil-induced mouse ear edema(inhibitory rateswere 26%-29% and 35%-59%,respectively). BR-H<sub>2</sub>O extract exhibited inhibitory effect incarrageenin,histamine and hot scald-inducedhind paw edema and adjuvant-induced arthritis inrats and cotton pellet-induced granulomaformation in mice.CONCLUSION BR extract exhibited inhibitory effect on formation of preneoplastic hepatic foci in early stage of rat chemical hepato-carcinogenesis. Both CH<sub>2</sub>CI<sub>2</sub> and H<sub>2</sub>O extracts from BR exerted anti-inflammatory effect in rats and mice.
文摘AIM To .investigate if sleep deprivation is able to increase the expression of inducible heat shock protein 70 in gastric mucosa and its possible role in mucosal defense.METHODS Rats for sleep disruption were placed inside a computerized rotating drum, gastric mucosa was taken from rats with 1, 3 and 7 d sleep deprivation. RT-PCR,immunohistochemistry and Western blotting were used to determine the expression of heat shock protein 70.Ethanol (500 mL@ L 1, I.g.) was used to induce gastric muceea damage.RESULTS RT-PCR, Western blotting and immunostaining confirmed that the sleep deprivation as a stress resulted in significantly greater expression of inducible heat shock protein 70 in gastric mucosa of rats. After the 500mL@ L-1 ethanol challenge, the ulcer area found in the rats with 7 d sleep deprivation (19.15 ± 4.2) mm2 was significantly lower (P<0.01) than the corresponding control (53.7 ± 8.1) mm2.CONCLUSION Sleep deprivation as a stress, in addition to lowering the gastric mucosal barrier, is able to stimulate the expression of inducible heat shock protein 70 in gastric mucosa of rats, the heat shock protein 70 may play an important role in gastric mucosal protection.
基金Supported by Special Scientific Research Program of Shaanxi Provincial Education Department(No.16JK1665)
文摘AIM:To assess the expression of nestin and glial fibrillary acidic protein(GFAP)in rat retina after optic nerve transection.METHODS:Rats were randomly divided into normal control group,sham group and operation group,and used for establishing an animal model of optic nerve transection.Retinal specimen of each group was collected at 3,48h,7and 14d postoperative.Nestin and GFAP expressions on sagittal sections were analyzed by immunohistochemical staining,and protein extraction was analyzed by Western blot.RESULTS:Immunohistochemical analysis showed that nestin positive staining was rarely detected in normal control group and sham group,while sham group showed weak positive staining at 3h postoperative,the reaction gradually increased at 48h postoperative,and reached its maximum at 7d postoperative,and then decreased at 14d postoperative.Compared to the expression of GFAP,there was not statistically significant obvious difference among three groups(P〉0.05).Result of Western blot method was consistent with that of immunohistochemical method.CONCLUSION:The expression of nestin increased in a time dependent fashion in Müller cells of retina following optic nerve transection,which was statistically significant,but there was no obvious difference in GFAP expression.The results indicate that an increase in colloid synthesis in retina following optic nerve transection can improve the retinal neurons’environment.
文摘Objective: To study the synthesis of heat shock pro- tein 70 (HSP70) by zinc ( ZnSO_4) and its protective effect during cold preservation in rat liver by estab- lishment of a simple cold preservation model. Methods: Wistar rats were divided into 5 groups (n =6): control group untreated before operation; Zn- 1, Zn-2, and Zn-3 groups treated before operation with zinc sulfate (Zn^(2+) 5 mg/kg, 10 mg/kg, 15 mg/ kg respectively); H group treated with heat shock (42.5 ℃×15 min). The livers of the rats were pre- served in UW solution for 6, 12, 24 hours. The re- sults of heat shock protein (HSP) synthesis were ana- lyzed with Western blot. The aspartate aminotrans- ferase (AST) and lactic dehydrogenase (LDH) values of perfusion and histological findings were evaluated. Results: A great amount of HSPs was synthesized af- ter pretreatment with zinc and heat shock. The AST and LDH values of the Zn-1, Zn-2 and H groups were significantly lower than those of the C group (P <0.05). But the value of the Zn-3 group was much higher. Histologically, mild injury was observed in the Zn-1, Zn-2 and H groups, but severe injury in the Zn-3 group. Conclusions: Zn^(2+), as a potent and feasible inducer of HSP expression, is able to protect the liver for cold preservation. Proper induction dosage of Zn^(2+) ranges from 5 mg/kg to 10 mg/kg, and Zn^(2+) 15 mg/ kg could not be a stress conditioning factor for its ad- verse effect on rat liver.
基金supported by the National Natural Science Foundation of China (30972512)the Graduate Innovation Fund of Academic Degree Committee Office of the Shanxi Provincial Government (20093014)+1 种基金Doctor Start-up Fund from Shanxi Medical University (B03201209)the College Students Innovation Fund of Shanxi Medical University (2010-25)
文摘Objective To investigate the impact of sub-chronic Aluminium-maltolate [Al(mal)s] exposure on the catabolism of amyloid precursor protein (APP) in rats. Methods Forty adult male Sprague-Dawley (SD) rats were randomly divided into five groups: the control group, the maltolate group (7.56 mg/kg BW), and the Al(mal)s groups (0.27, 0.54, and 1.08 mg/kg BW, respectively). Control rats were administered with 0.9% normal saline through intraperitoneal (i.p.) injection. Maltolate and Al(mal)s were administered to the rats also through i.p. injections. Administration was conducted daily for two months. Rat neural behavior was examined using open field tests (OFT). And the protein expressions and their mRNAs transcription related with APP catabolism were studied using enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (RT-PCR). Results The expressions of APP, 13-site APP cleaving enzyme 1 (BACEI) and presenilin-1 (PSi) proteins and their mRNAs transcription increased gradually with the increase of Al(mal)3 doses (P〈0.05). The enzyme activity of BACEI in the 0.54 and 1.08 mg/kg Al(mal)s groups increased significantly (P〈0.05). The expression of 8-amyloid protein (AS) 1-40 gradually decreased while the protein expression of A81-42 increased gradually with the increase of Al(mal)s doses (P〈0.05). Conclusion Result from our study suggested that one of the possible mechanisms that Al(mal)s can cause neurotoxicity is that Al(mal)s can increase the generation of A81-42 by facilitating the expressions of APP, β-, and γ-secretase.
基金Supported by Natural Science Fundation of Hainan Province 2008(No 30855)
文摘Objective:To investigate the expression of Runx3 and TGF-β<sub>1</sub> protein in the colon from rats with irritable bowel syndrome(IBS).Methods:Rat model for IBS was established by intracolonic instillation with acetic acid and restraint stress methods,which was confirmed by determinating the visceral sensitivity of the animals,including abdominal withdrawal reflex (AWR) score and the electronic behavior of the abdomen wall.The rats were randomly assigned into three groups:IBS,group(restraint stress,n=25);IBS<sub>2</sub> group(both instillation with acetic acid and restraint stress,n=25) and Control group(n=16).The colonic tissue samples were collected for histological study and the expression of Runx3 and TGF-β<sub>1</sub> proteins were detected by immunohistochemistry.Meanwhile,the relationship of these two proteins was calculated. Results:Visceral hypersensitivity(AWR and abdominal electrical activity) was significantly enhanced in IBS,and IBS<sub>2</sub> groups than other groups.The colon tissue in all groups did not show any signs of inflammation.Furthermore,the expression of Runx3 and TGF-β<sub>1</sub> protein in the colon from all groups show no significant difference(P】0.05),with no remarkable relevancy between each other(P】0.05).Conclusions:The rat model for IBS was successfully established. We did not find any significant changes in the expression of Runx3 and TGF-β<sub>1</sub> protein in the colon tissue from IBS rats,suggesting that the quantitative changes may be not the way by which Runx3 and TGF-β<sub>1</sub> protein play their roles in IBS.The accurate roles of Runx3 and TGF-β<sub>1</sub> proteins in the pathogenesis of IBS remains to be further studied.
文摘Previous studies have suggested that glutathione-S-transferase π (GST-π) over-expression in the brain tissue is associated with refractory epilepsy. However, whether the change in GST-π level in the peripheral blood is in line with that in brain tissue remains unknown. This study examined the correlation between GST-π in brain tissue and that in peripheral blood in rat models of pilocarpine-induced refractory epilepsy. The animals were divided into drug-resistant group and drug-responsive group according to the response to anti-epileptic drugs. GST-π expression in brain tissue was immunohistochemically determined, while the expression of GST-π in peripheral blood was analyzed by Western blotting. In the hippocampus and cortex, GST-π was mainly found in the cytoplasm and membrane of neurons, and the GST-π expression level was higher in drug-resistant group than in the drug-responsive group and saline control group (P〈0.05). Moreover, there was no significant difference between responders and saline control animals (P〉0.05). The change in expression of GST-π in peripheral blood showed the same pattern as that in brain tissues, suggesting GST-π might contribute to drug resistance in epilepsy. Importantly, the GST-π over-expression in peripheral blood could be used as a marker for resistance to anti-epileptic agents.
文摘Objective :To elucidate whether cell multiplication, apoptosis, glucose intake and p-Akt protein expression of bone Mesenchyreal Stem Cells(MSCs) of rats is influenced by a hypoxic environment ex vivo. Methods :Passage 3 of bone marrow MSCs taken from Wistar rats,were cultured in a culturing chamber with 94%N2,1%O2,5%CO2 at 37℃. At different hypoxia time points ,0,0.5, 1,4 and 8 h, glucose uptake was assayed by using radiation isotope ^3H-G, Apoptotic Rate(AR) and dead rate(DR) were analyzed by flow cytometry(FCM) after Annexin V/PI staining, cell multiplication(by MTr methods) and p-Akt protein by immunocytochemistry and western blot. Results :Assay for CD29^± ,CD44^± ,CD71^± ,CD34^-, Tn T^±(after 5-azacytidine agent inducing) and ALP^±(after bone differentiation agent inducing) suggested these bone-derived cells were MSCs. The ^3H-G intaking ratio (CPM/ flask value:157 ± 11,110 ± 11,107 ± 13,103 ± 10,100 ± 9 and 98 ± 10) of MSCs at different hypoxia time points, significantly decreased compared to that of normoxia(P 〈 0.01) and tended to descend slowly with hypoxia time duration, for which there was no statistical significance(P 〉 0.05). The AR(0.09 ± 2.03%,12.9 ± 1.72%,13.7 ± 2.26%,13.8 ± 3.01%,14.1 ± 2.78% and 14.7 ± 4.01% at 0,0.5,1,4 and 8 h,respectively,P 〈 0.01) and DR (0.04, ± 1.79% ,0.93 ± 1.85% ,3.11 ± 2.14% ,4.09 ± 2.36% ,4.72 ± 2.05% and 4.91 ± 3.72% at 0,0.5,1,4 and 8 h, respectively, P 〈 0.05) at different hypoxia time points significantly increased compared to those time in normoxia; The AR further went up with time (P 〈 0.05), however there was no statistical significance (P 〉 0.05) for the DR. Optical absorption value of MTr methods at different hypoxia time points significantly decreased compared to those with a corresponding normoxia time (P 〈 0.01) and degraded with time (in an hypoxic environment -P 〈 0.01). IOD of p-Akt protein of MSCs at different hypoxia time points significantly increased (0.367 ± 0.031,0.556 ± 0.023,0.579 ± 0.013, 0.660 ± 0.024, 0.685 ± 0.039 and 0.685 ± 0.011, respectively) compared to their equivalents in normoxia (P〈0.05), however, there was no statistical significance (P 〉 0.05) for different hypoxia time points. Hypoxia may result in ultramicrostructure changes, such as defluvium of Microvilli, apoptotic body, "margination" and so on and are further aggravated with hypoxia time stretching. Conclusion: Hypoxia may lead to a depression of MSCs intaldng glucose, creep of cell multiplication, upregulation of p-Akt protein and apoptosis of MSCs ex vivo.
基金supported by a grant from Luzhou Medical College,China
文摘This study aimed to explore the pathological change to hippocampal neurons and the expression of growth associated protein 43 in 21-day-old young rats following chronic intermittent hypoxia. Hematoxylin-eosin staining results showed varying degrees of degeneration and necrosis in hippocampal neurons depending on the modeling time. Immunohistochemistry revealed that growth associated protein 43 expression in young rats following chronic intermittent hypoxia decreased, but that levels were still higher than those of normal rats at each time point, especially 4 weeks after modeling. During 1 5 weeks after modeling, a slow growth in rat weight was observed. Experimental findings indicate that chronic intermittent hypoxia may induce growth dysfunction and necrosis of hippocampal neurons, as well as increase the expression of growth associated protein 43 in young rats.
基金National Natural Science Foundation of China,No.81704059Scientific Research Project of Hebei Province Traditional Chinese Medicine Administration,No.2017130。
文摘BACKGROUND Intestinal inflammation is a common digestive tract disease, which is usually treated with hormone medicines. Hormone medicines are effective to some extent, but long-term use of them may bring about many complications.AIM To explore the protective effects of panax notoginseng saponin(PNS) against dextran sulfate sodium(DSS)-induced intestinal inflammatory injury through phosphoinositide-3-kinase protein kinase B(PI3K/AKT) signaling pathway inhibition in rats.METHODS Colitis rat models were generated via DSS induction, and rats were divided into control(no modeling), DSS, DSS + PNS 50 mg/k, and DSS + PNS 100 mg/kg groups. Then, the intestinal injury, oxidative stress parameters, inflammatory indices, tight junction proteins, apoptosis, macrophage polarization, and TLR4/AKT signaling pathway in colon tissues from rats in each of the groups were detected. The PI3 K/AKT signaling pathway in the colon tissue of rats was blocked using the PI3K/AKT signaling pathway inhibitor, LY294002.RESULTS Compared with rats in the control group, rats in the DSS group showed significantly shortened colon lengths, and significantly increased disease activity indices, oxidative stress reactions and inflammatory indices, as well as significantly decreased expression of tight junction-associated proteins. In addition, the DSS group showed significantly increased apoptotic cell numbers,and showed significantly increased M1 macrophages in spleen and colon tissues.They also showed significantly decreased M2 macrophages in colon tissues, as well as activation of the PI3K/AKT signaling pathway(all P < 0.05). Compared with rats in the DSS group, rats in the DSS + PNS group showed significantly lengthened colon lengths, decreased disease activity indices, and significantly alleviated oxidative stress reactions and inflammatory responses. In addition, this group showed significantly increased expression of tight junction-associated proteins, significantly decreased apoptotic cell numbers, and significantly decreased M1 macrophages in spleen and colon tissues. This group further showed significantly increased M2 macrophages in colon tissues, and significantly suppressed activation of the PI3K/AKT signaling pathway, as well as a dose dependency(all P < 0.05). When the PI3K/AKT signaling pathway was inhibited, the apoptosis rate of colon tissue cells in the DSS + LY294002 group was significantly lower than that of the DSS group(P < 0.05).CONCLUSION PNS can protect rats against DSS-induced intestinal inflammatory injury by inhibiting the PI3K/AKT signaling pathway, and therefore may be potentially used in the future as a drug for colitis.
基金the National Natural Science Foundation of China,No.30900773the National University Basic Research Foundation of China,No.2010QZZD022
文摘Previous studies have reported that non-human primates and rodents exposed to lead during brain development may become dependent on the deposition of pre-determined β-amyloid protein (Aβ),and exhibit upregulation of β-site amyloid precursor protein expression in old age.However,further evidence is required to elucidate the precise relationship and molecular mechanisms underlying the effects of early lead exposure on excessive Aβ production in adult mammals.The present study investigated the effects of lead exposure on expression of β-amyloid precursor protein cleavage enzyme-1 (BACE-1) in the rat retina and the production of Aβ in early development,using the retina as a window for studying Alzheimer's disease.Adult rats were intraocularly injected with different doses of lead acetate (10μmol/L,100μmol/L,1 mmol/L,10 mmol/L and 100 mmol/L).The results revealed that retinal lead concentration,BACE-1 and its cleavage products β-C-terminal fragment and retina Aβ1-40 were all significantly increased in almost all of the lead exposure groups 48 hours later in a dose-dependent manner.The only exception was the 10μmol/L group.The distribution of BACE-1 in the retina did not exhibit obvious changes,and no distinctive increase in the activation of retinal microglia was apparent.Similarly,retinal synaptophysin expression did not exhibit any clear changes.These data suggest that lead exposure can result in the upregulation of retinal neuron BACE-1 expression in the early period of development and further increase the overproduction of Aβ1-40 in the retina.Our results provided novel insight into the molecular mechanisms underlying environmentally-induced Alzheimer's disease.
文摘All motions provide sensory, motoric, and reflexive input to the central nervous system, as well as playing an important role in cerebral functional plasticity and compensation. Cerebral plasticity has become the theoretical basis of neurorehabilitation. Studies of cerebrovascular disease, in particular, demonstrate that regeneration is accompanied by multiple forms of plasticity, such as functional and structural, in different phases of stroke rehabilitation. This study was designed to measure synaptic plasticity and expression of associated proteins to analyze the effect of rehabilitation training on learning and memory in a rat model of cerebral infarction. Results suggest that rehabilitation training increases expression of nerve growth factor associated protein 43, brain-derived neurotrophic factor, and neural cell adhesion molecules, and also promotes cerebral functional plasticity.
基金the National Natural Science Foundation of China, No. 30973732
文摘A previous study from our group showed that Jiawei Wendan decoction inhibits protein expression of interleukin-1β, 2, and 6, as well as plasma neuropeptide Y, P substance and somatostatin in the hippocampus of depression rat models. The present study analyzed the influence of Jiawei Wendan decoction on the mitogen-activated protein kinase signal transduction pathway in the hippocampus. Results demonstrated that Jiawei Wendan decoction effectively upregulated expression of small molecular G proteins, extracellular regulated kinase 1/2, and activated ribosomal S6 kinase protein in the rat hippocampus. In addition, Jiawei Wendan decoction exhibits antidepressant effects similar to fluoxetine. The underlying mechanisms were shown to be dependent on increased mitogen-activated protein kinase signal transduction pathway activity.
文摘Objective To study whether there is the apoptosis of neural cells and the expression of Bcl-2 protein in intracerebral hemorrhage (ICH) in model of rats, for the further understanding the mechanism of the delayed damage of the neural cells around the hematoma after ICH. Methods Fifty SD rats were randomly divided into 5 groups, ten in each. With the Group A as the control, the rest 40 were used to set up intracerebral hemorrhage model. The brains were taken out at 12 th , 24 th , 48 th and 72 th hours, respectively. Apoptosis cells were detected with terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL), and the expression of Bcl-2 protein was detected with immunochemical stainging methed (SP). Results In the control group, no apoptosis cells and Bc1-2 protein were detected. In rest groups, the apoptosis cells and Bc1-2 protein were expressed in different degree. Apoptosis rates verified and corresponded with the time after ICH, with the peak at 48 th -72 th hour after hemorrhage. The peak rate of apoptosis cells was (24.50±2.69)% and Bcl-2 protein expression was (20.76±1.97)% . There was significant difference between the experimental groups and control (P<0.05), and no linear relationship between the apoptosis rate and the expression of Bcl-2 protein. Conclusion Apoptosis may be an important factor in the secondary trauma of ICH. There is a time leg after hemorrhage. All this is instructive to clinical treatment in time. Bcl-2 protein keeps increasing in a certain time after hemorrhage, but not synchronize with the cell apoptosis. This indicates that bcl-2 has the effect to reduce the apoptosis of neural cells.
基金supported by Brazilian funding agencies CNPq,CAPES and FAPERGS
文摘Emerging evidence has suggested global histone H4 acetylation status plays an important role in neural plasticity. For instance, the imbalance of this epigenetic marker has been hypothesized as a key factor for the development and progression of several neurological diseases. Likewise, astrocytic reactivity-a wellknown process that markedly influences the tissue remodeling after a central nervous system injury-is crucial for tissue remodeling after spinal cord injury(SCI). However, the linkage between the above-mentioned mechanisms after SCI remains poorly understood. We sought to investigate the relation between both glial fibrillary acidic protein(GFAP) and S100 calcium-binding protein B(S100B)(astrocytic reactivity classical markers) and global histone H4 acetylation levels. Sixty-one male Wistar rats(aged ~3 months) were divided into the following groups: sham; 6 hours post-SCI; 24 hours post-SCI; 48 hours post-SCI; 72 hours post-SCI; and 7 days post-SCI. The results suggested that GFAP, but not S100B was associated with global histone H4 acetylation levels. Moreover, global histone H4 acetylation levels exhibited a complex pattern after SCI, encompassing at least three clearly defined phases(first phase: no changes in the 6, 24 and 48 hours post-SCI groups; second phase: increased levels in the 72 hours post-SCI group; and a third phase: return to levels similar to control in the 7 days post-SCI group). Overall, these findings suggest global H4 acetylation levels exhibit distinct patterns of expression during the first week post-SCI, which may be associated with GFAP levels in the perilesional tissue. Current data encourage studies using H4 acetylation as a possible biomarker for tissue remodeling after spinal cord injury.
基金the National Natural Science Foundation of China, No. 30471917the Hong Kong Research Grant Council,No. HKU 7198/01
文摘BACKGROUND: High incidence of stroke at interchange period of autumn and winter was demonstrated by epidemiological survey, and the specific causes should be further investigated. OBJECTIVE: To investigate the influence of artificial cold exposure on the incidence of stroke in renovascular hypertensive rats (RHR), and analyze the association with blood pressure and cold-inducible RNA binding protein (CIRP) mRNA expression in brain tissue. DESIGN: A completely randomized grouping design, a randomized control animal trial. SETTINGS: Lab of Neurology, the First Affiliated Hospital of Sun Yat-sen University; Department of Chemistry, Open laboratory of Chemical Biology, Institute of Molecular Technology for Drug Discovery and Synthesis, University of Hong Kong. MATERIALS: Male SD rats (n=460), weighing 80 - 100 g were obtained from Guangdong Province Health Animal Unit. A modified RXZ-300A intelligent artificial climate cabinet (Ningbo Jiangnan Instrument Co. ,Ltd., China). METHODS: The experiment were processed in the Lab of Neurology, the First Affiliated Hospital of Sun Yat-sen University and the Open Laboratory of Chemical Biology, Institute of Molecular Technology for Drug Discovery and Synthesis, University of Hong Kong from October 2004 to November 2005. Rats (n = 400) were operated to establish 2-kidney 2-clip RHR model as described previously. The sham-operated rats (n =60) served as normotensive controls. Eight weeks later, 300 of RHR were randomly selected according to their systolic blood pressure (SBP) and divided into 3 sub-groups (n =100 per group): mild hypertensive group (SBP of 160 - 200 mm Hg), moderate hypertensive group (SBP of 200 - 220 mm Hg) and severe hypertensive group (SBP 〉 220 mm Hg). Each group was further divided into two groups (n =50) under ACE and non-ACE. Normal sham-operated SD rats (n =60), SBP 〈 140 mm Hg, were randomly divided into two groups: Sham-operated control group (n =30) under ACE and non-ACE. To establish the ACE and non-ACE treatment, rats were housed individually in artificial climate cabinet, and ACE was designed as three cycles of 12-hour light of 22℃ (7 : 00 - 19 : 00) and 12-hour dark of 4℃(19 : 00 - 7 : 00). The non-ACE group was kept at 22℃ throughout the experiment. MAIN OUTCOME MEASURES: Blood Pressure changes were measured and stroke symptom were observed; Expression of the CIRP were examined by reverse transcription-polymerase chain reaction. RESULTS: Finally 360 rats were involved in the analysis of results. ①Incidence of stroke: The incidence of stroke in 2k2c RHR was significantly higher after a three-day intermittent (12-hour) ACE (29.3%) as compared with that in non-ACE (17.3%) (P 〈 0.05). Furthermore, the severe hypertensive 2k2c RHR (BP 〉 220 mm Hg) was found to have much higher incidence of stroke (66%, 33/50) than the mild (8%, 4/50) and moderate (18%) hypertensive 2k2c RHR. ②CIRP mRNA in brain tissue: ACE treatment stimulated the mRNA expression of CIRP in non-stroke 2k2c RHR but not in stroke 2k2c RHR (P 〈 0.05). CONCLUSION: High blood pressure and low expression of CIRP are associated with ACE induced stroke.
文摘Approximately 40-50 β-defensins are predominantly expressed in the male reproductive system of mammals. This selective expression raises the question as to the roles of these molecules in innate immunity and fertility in the male reproductive tract. Rat β-defensin 22 is an epididymis-specific β-defensin expressed in segments 12-14 of the epididymis. This protein contains both β-defensin and lectin signature sequences, yet its antimicrobial activity and carbohydrate-binding ability have not been shown. We herein demonstrated the antimicrobial activity of recombinant rat β-defensin 22 against Escherichia coliand Candida albicans. Its lectinJike activity was also investigated by demonstrating its binding ability with heparin beads. This heparin-binding activity implies some potential roles for this defensin in determining the fertilisation capabilities of sperm.