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Semaphorin 7A impairs barrier function in cultured human corneal epithelial cells in a manner dependent on nuclear factor-kappa B
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作者 Cheng-Cheng Yang Xiu-Xia Yang +5 位作者 Xiao-Jing Zhao Heng Wang Zi-Han Guo Kai Jin Yang Liu Bin-Hui Li 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2024年第3期444-453,共10页
●AIM:To evaluate the role of semaphorin 7A(Sema7A)and its associated regulatory mechanisms in modulating the barrier function of cultured human corneal epithelial cells(HCEs).●METHODS:Barrier models of HCEs were tre... ●AIM:To evaluate the role of semaphorin 7A(Sema7A)and its associated regulatory mechanisms in modulating the barrier function of cultured human corneal epithelial cells(HCEs).●METHODS:Barrier models of HCEs were treated with recombinant human Sema7A at concentrations of 0,125,250,or 500 ng/mL for 24,48,or 72h in vitro.Transepithelial electrical resistance(TEER)as well as Dextran-fluorescein isothiocyanate(FITC)permeability assays were conducted to assess barrier function.To quantify tight junctions(TJs)such as occludin and zonula occludens-1(ZO-1)at the mRNA level,reverse transcriptionpolymerase chain reaction(RT-PCR)analysis was performed.Immunoblotting was used to examine the activity of the nuclear factor-kappa B(NF-κB)signaling pathway and the production of TJs proteins.Immunofluorescence analyses were employed to localize the TJs.Enzyme-linked immunosorbent assay(ELISA)and RT-PCR were utilized to observe changes in interleukin(IL)-1βlevels.To investigate the role of NF-κB signaling activation and IL^(-1)βin Sema7A’s anti-barrier mechanism,we employed 0.1μmol/L IκB kinase 2(IKK2)inhibitor IV or 500 ng/mL IL^(-1)receptor(IL-1R)antagonist.●RESULTS:Treatment with Sema7A resulted in decreased TEER and increased permeability of Dextran-FITC in HCEs through down-regulating mRNA and protein levels of TJs in a time-and dose-dependent manner,as well as altering the localization of TJs.Furthermore,Sema7A stimulated the activation of inhibitor of kappa B alpha(IκBα)and expression of IL-1β.The anti-barrier function of Sema7A was significantly suppressed by treatment with IKK2 inhibitor IV or IL-1R antagonists.●CONCLUSION:Sema7A disrupts barrier function through its influence on NF-κB-mediated expression of TJ proteins,as well as the expression of IL-1β.These findings suggest that Sema7A could be a potential therapeutic target for the diseases in corneal epithelium. 展开更多
关键词 human corneal epithelial barrier function transepithelial electrical resistance zonula occludens-1 OCCLUDIN nuclear factor-kappa b
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Inhibitory effects of Shuanghuanglian injection on nuclear factor-kappa B expression in mice with viral encephalitis in a time-and dose-dependent manner 被引量:1
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作者 Ye Tian Caiping Han Naibing Gu Zhengli Di Gejuan Zhang Hui Lei 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第24期1865-1869,共5页
Previous studies have confirmed that the anti-virus effects of Shuanghuanglian injection may be associated with nuclear factor-kappa B activity. This study observed nuclear factor-kappa B expression in mice with viral... Previous studies have confirmed that the anti-virus effects of Shuanghuanglian injection may be associated with nuclear factor-kappa B activity. This study observed nuclear factor-kappa B expression in mice with viral encephalitis, and showed significant decreases in nuclear factor-kappa B protein and mRNA levels following Shuanghuanglian injection. The inhibitory effect was more significant with prolonged intervention duration and increased treatment dose. These findings verify that Shuanghuanglian injection plays a therapeutic role in viral encephalitis by reducing expression of nuclear factor-kappa B in a time- and dose-dependent manner. 展开更多
关键词 nuclear factor-kappa b viral encephalitis MICE gene expression Shuanghuanglian injection neural regeneration
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Delayed hepatocarcinogenesis through antiangiogenic intervention in the nuclear factor-kappa B activation pathway in rats 被引量:31
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作者 Dong, Zhi-Zhen Yao, Deng-Fu +7 位作者 Wu, Wei Yao, Min Yu, Hong-Bo Shen, Jun-Jun Qiu, Li-Wei Yao, Ning-Hua Sai, Wen-Li Yang, Jun-Ling 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2010年第2期169-174,共6页
BACKGROUND: The active form of nuclear factor-kappa B (NF-kappa B) is involved in the initiation, generation, and development of hepatocellular carcinoma (HCC), and is up-regulated in inflammation-associated malignanc... BACKGROUND: The active form of nuclear factor-kappa B (NF-kappa B) is involved in the initiation, generation, and development of hepatocellular carcinoma (HCC), and is up-regulated in inflammation-associated malignancies. We investigated the dynamic expression of NF-kappa B and its influences on the occurrence of HCC through antiangiogenic (thalidomide) intervention in NF-kappa B activation. METHODS : Hepatoma models were induced with 2-fluorenylacetamide (2-FAA, 0.05%) in male Sprague-Dawley rats, and thalidomide (100 mg/kg body weight) was administered intragastrically to intervene in NF-kappa B activation. The pathological changes in the liver of sacrificed rats were assessed after hematoxylin and eosin staining. NF-kappa B mRNA was amplified by RT-nested PCR. The alterations of NF-kappa B and vascular endothelial growth factor (VEGF) expression were analyzed by enzyme-linked immunosorbent assay, immunohistochemistry, and Western blotting. RESULTS: Rat hepatocytes showed denatured, precancerous, and cancerous stages in hepatocarcinogenesis, with an increasing tendency of hepatic NF-kappa B, NF-kappa B mRNA, and VEGF expression, and their values in the HCC group were higher than those in controls (P<0.001). In the thalidomide-treated group, the morphologic changes generated only punctiform denaturation and necrosis at the early or middle stages, and nodular hyperplasia or a little atypical hyperplasia at the final stages, with the expression of NF-kappa B (chi(2)=9.93, P<0.001) and VEGF (chi(2)=8.024, P<0.001) lower than that in the 2-FAA group. CONCLUSION: NF-kappa B is overexpressed in hepatocarcinogenesis and antiangiogenic treatment down-regulates the expression of NF-kappa B and VEGF, and delays the occurrence of HCC. (Hepatobiliary Pancreat Dis Int 2010; 9: 169-174) 展开更多
关键词 hepatocellular carcinoma nuclear factor-kappa b vascular endothelial growth factor INTERVENTION dynamic expression
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Urinary trypsin inhibitor attenuates hepatic ischemia-reperfusion injury by reducing nuclear factor-kappa B activation 被引量:28
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作者 Wu, Yi-Jun Ling, Qi +4 位作者 Zhou, Xin-Hui Wang, Yan Xie, Hai-Yang Yu, Ji-Ren Zheng, Shu-Sen 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2009年第1期53-58,共6页
BACKGROUND: Urinary trypsin inhibitor (UTI) inhibits the inflammatory response and protects against ischemia-reperfusion (I/R) injury. The inflammatory response is mediated by nuclear factor-kappa B (NF-kappa B) and i... BACKGROUND: Urinary trypsin inhibitor (UTI) inhibits the inflammatory response and protects against ischemia-reperfusion (I/R) injury. The inflammatory response is mediated by nuclear factor-kappa B (NF-kappa B) and its related target genes and products such as vascular endothelial cell adhesion molecule and CXC chemokines. We aimed to assess the roles of those mediators in a UTI-treated mouse model of hepatic I/R injury. METHODS: Treatment group 1 (UTI given 5 minutes prior to liver ischemia), treatment group 2 (UTI given 5 minutes after the anhepatic phase) and a control group were investigated. Blood and liver samples were obtained and compared at 1, 3, 6 and 24 hours after reperfusion. RESULTS: Attenuation of pathological hepatocellular damage was greater in the treatment groups than in the control group (P < 0.05). Compared with the control group, the UTI treatment groups showed significantly lower serum alanine aminotransferase and aspartate aminotransferase levels, decreased myeloperoxidase activity, and reduced NF-kappa B activation. Also downregulated was the expression of tumor necrosis factor-alpha, cytokine-induced neutrophil chemoattractant, and macrophage inflammatory protein-2 at the mRNA level. P-selectin protein and intercellular adhesion molecule-1 protein expression were also downregulated. In addition, the treatment group I showed a better protective effect against I/R injury than the treatment group 2. CONCLUSIONS: UTI reduces NF-kappa B activation and downregulates the expression of its related mediators, followed by the inhibition of neutrophil aggregation and infiltration in hepatic I/R injury. The protective role of UTI is more effective in prevention than in treatment. 展开更多
关键词 ischemia-reperfusion injury nuclear factor-kappa b tumor necrosis factor-alpha urinary trypsin inhibitor
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Characteristics of hepatic nuclear-transcription factor-kappa B expression and quantitative analysis in rat hepatocarcinogenesis 被引量:12
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作者 Wu, Wei Yao, Deng-Fu +7 位作者 Qiu, Li-Wei Sai, Wen-Li Shen, Jun-Jun Yu, Hong-Bo Wu, Xin-Hua Li, Yue-Ming Wang, Yi-Lang Gu, Wen-Jing 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2009年第5期504-509,共6页
BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors. We analyzed the expression of miclear-transcription factor-kappa B (NF-kappa B) during hepatocarcinogenesis in order to evaluate i... BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors. We analyzed the expression of miclear-transcription factor-kappa B (NF-kappa B) during hepatocarcinogenesis in order to evaluate its dynamic expression and its clinical value in the development and diagnosis of HCC. METHODS: Hepatoma models were induced by oral administration of 2-acetamidoflurene (2-FAA) to male Sprague-Dawley rats. Morphological changes were observed after hematoxylin and eosin staining. The cellular distribution of NF-kappa B expression during different stages of cancer development was investigated by immunohistochemistry, and the level of NF-kappa B expression in liver tissues was quantitatively analyzed by ELISA. The gene fragments of hepatic NF-kappa B were amplified by nested-polymerase chain reaction assay. RESULTS: Hepatocytes showed vacuole-like degeneration during the early stages, then had a hyperplastic nodal appearance during the middle stages, and finally progressed to tubercles of cancerous nests with high differentiation. The NF-kappa B-positive material was buff-colored, fine particles localized in the nucleus, and the incidence of NF-kappa B-positive cells was 81.8% in degeneration, 83.3% in precancerous lesions, and 100% in cancerous tissues. All of these values were higher than those in controls (P<0.01). Hepatic NF-kappa B expression and hepatic NF-kappa B-mRNA were also higher during the course of HCC development (P<0.01). CONCLUSION: The NF-kappa B signal transduction pathway is activated during the early stages of HCC development, and its abnormal expression may be associated with the occurrence of HCC. 展开更多
关键词 hepatocellular carcinoma nuclear factor-kappa b IMMUNOHISTOCHEMISTRY nested-polymerase chain reaction NF-kappa b-mRNA
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Dietary saturated fatty acid and polyunsaturated fatty acid oppositely affect hepatic NOD-like receptor protein 3 inflammasome through regulating nuclear factor-kappa B activation 被引量:11
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作者 Yong-heng Sui Wen-jing Luo +1 位作者 Qin-Yu Xu jing hua 《World Journal of Gastroenterology》 SCIE CAS 2016年第8期2533-2544,共12页
AIM: To investigate the effect of different dietary fatty acids on hepatic inflammasome activation.METHODS: Wild-type C57BL/6 mice were fed either a high-fat diet or polyunsaturated fatty acid (PUFA)-enriched diet. Pr... AIM: To investigate the effect of different dietary fatty acids on hepatic inflammasome activation.METHODS: Wild-type C57BL/6 mice were fed either a high-fat diet or polyunsaturated fatty acid (PUFA)-enriched diet. Primary hepatocytes were treated with either saturated fatty acids (SFAs) or PUFAs as well as combined with lipopolysaccharide (LPS). The expression of NOD-like receptor protein 3 (NLRP3) inflammasome, peroxisome proliferator-activated receptor-&#x003b3; and nuclear factor-kappa B (NF-&#x003ba;B) was determined by real-time PCR and Western blot. The activity of Caspase-1 and interleukine-1&#x003b2; production were measured.RESULTS: High-fat diet-induced hepatic steatosis was sufficient to induce and activate hepatic NLRP3 inflammasome. SFA palmitic acid (PA) directly activated NLRP3 inflammasome and increased sensitization to LPS-induced inflammasome activation in hepatocytes. In contrast, PUFA docosahexaenoic acid (DHA) had the potential to inhibit NLRP3 inflammasome expression in hepatocytes and partly abolished LPS-induced NLRP3 inflammasome activation. Furthermore, a high-fat diet increased but PUFA-enriched diet decreased sensitization to LPS-induced hepatic NLRP3 inflammasome activation in vivo. Moreover, PA increased but DHA decreased phosphorylated NF-&#x003ba;B p65 protein expression in hepatocytes.CONCLUSION: Hepatic NLRP3 inflammasome activation played an important role in the development of non-alcoholic fatty liver disease. Dietary SFAs and PUFAs oppositely regulated the activity of NLRP3 inflammasome through direct activation or inhibition of NF-&#x003ba;B. 展开更多
关键词 Non-alcoholic fatty liver disease NOD-like receptor protein 3 inflammasome Saturated fatty acids Polyunsaturated fatty acids nuclear factor-kappa b
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Testosterone alleviates tumor necrosis factor-alpha-mediated tissue factor pathway inhibitor downregulation via suppression of nuclear factor-kappa B in endothelial cells 被引量:2
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作者 Hong Jin Wen-Bing Qiu +4 位作者 Yi-Fang Mei Qin Zhang Dong-Ming Wang Yu-Guang Li Xue-Rui Tan 《Asian Journal of Andrology》 SCIE CAS CSCD 2009年第2期266-271,共6页
We have observed earlier that testosterone at physiological concentrations can stimulate tissue factor pathway inhibitor(TFPI)gene expression through the androgen receptor in endothelial cells.This study further inves... We have observed earlier that testosterone at physiological concentrations can stimulate tissue factor pathway inhibitor(TFPI)gene expression through the androgen receptor in endothelial cells.This study further investigated the impact of testosterone on TFPI levels in response to inflammatory cytokine tumor necrosis factor-alpha(TNF-α).Cultured human umbilical vein endothelial cells were incubated in the presence or absence of testosterone or TNF-α.TFPI protein and mRNA levels were assessed by enzyme-linked immunosorbent assay and quantitative real-time reverse transcription polymerase chain reaction.To study the cellular mechanism of testosterone’s action,nuclear factor-kappa B(NF-κB)translocation was confirmed by electrophoretic mobility shift assays.We found that after NF-κB was activated by TNF-α,TFPI protein levels declined significantly by 37.3%compared with controls(P<0.001),and the mRNA levels of TFPI also decreased greatly(P<0.001).A concentration of 30 nmol L-1 testosterone increased the secretion of TFPI compared with the TNF-α-treated group.NF-κB DNA-binding activity was significantly suppressed by testosterone(P<0.05).This suggests that physiological testosterone concentrations may exert their antithrombotic effects on TFPI expression during inflammation by downregulating NF-κB activity. 展开更多
关键词 nuclear factor-kappa b TESTOSTERONE tissue factor pathway inhibitor
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Jianpi Gushen Huayu decoction ameliorated diabetic nephropathy through modulating metabolites in kidney,and inhibiting TLR4/NF-κB/NLRP3 and JNK/P38 pathways 被引量:1
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作者 Zi-Ang Ma Li-Xin Wang +8 位作者 Hui Zhang Han-Zhou Li Li Dong Qing-Hai Wang Yuan-Song Wang Bao-ChaoPan Shu-Fang Zhang Huan-Tian Cui Shu-Quan Lv 《World Journal of Diabetes》 SCIE 2024年第3期502-518,共17页
BACKGROUND Jianpi Gushen Huayu Decoction(JPGS)has been used to clinically treat diabetic nephropathy(DN)for many years.However,the protective mechanism of JPGS in treating DN remains unclear.AIM To evaluate the therap... BACKGROUND Jianpi Gushen Huayu Decoction(JPGS)has been used to clinically treat diabetic nephropathy(DN)for many years.However,the protective mechanism of JPGS in treating DN remains unclear.AIM To evaluate the therapeutic effects and the possible mechanism of JPGS on DN.METHODS We first evaluated the therapeutic potential of JPGS on a DN mouse model.We then investigated the effect of JPGS on the renal metabolite levels of DN mice using non-targeted metabolomics.Furthermore,we examined the effects of JPGS on c-Jun N-terminal kinase(JNK)/P38-mediated apoptosis and the inflammatory responses mediated by toll-like receptor 4(TLR4)/nuclear factor-kappa B(NF-κB)/NOD-like receptor family pyrin domain containing 3(NLRP3).RESULTS The ameliorative effects of JPGS on DN mice included the alleviation of renal injury and the control of inflammation and oxidative stress.Untargeted metabolomic analysis revealed that JPGS altered the metabolites of the kidneys in DN mice.A total of 51 differential metabolites were screened.Pathway analysis results indicated that nine pathways significantly changed between the control and model groups,while six pathways significantly altered between the model and JPGS groups.Pathways related to cysteine and methionine metabolism;alanine,tryptophan metabolism;aspartate and glutamate metabolism;and riboflavin metabolism were identified as the key pathways through which JPGS affects DN.Further experimental validation showed that JPGS treatment reduced the expression of TLR4/NF-κB/NLRP3 pathways and JNK/P38 pathway-mediated apoptosis related factors.CONCLUSION JPGS could markedly treat mice with streptozotocin(STZ)-induced DN,which is possibly related to the regulation of several metabolic pathways found in kidneys.Furthermore,JPGS could improve kidney inflammatory responses and ameliorate kidney injuries in DN mice via the TLR4/NF-κB/NLRP3 pathway and inhibit JNK/P38 pathwaymediated apoptosis in DN mice. 展开更多
关键词 Diabetic nephropathy Jianpi Gushen Huayu Decoction Oxidative stress Inflammation Untargeted metabolomics Toll-like receptor 4/nuclear factor-kappa b/NOD-like receptor family pyrin domain containing 3 pathway c-Jun N-terminal kinase/P38-mediated apoptosis
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Shuanghuanglian injection downregulates nuclear factor-kappa B expression in mice with viral encephalitis 被引量:7
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作者 Naibing Gu Ye Tian +3 位作者 Zhengli Di Caiping Han Hui Lei Gejuan Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第33期2592-2599,共8页
A mouse model of viral encephalitis was induced by intracranial injection of a Coxsackie virus B3 suspension. Quantitative real-time reverse transcription-PCR and western blot assay were applied to detect mRNA and pro... A mouse model of viral encephalitis was induced by intracranial injection of a Coxsackie virus B3 suspension. Quantitative real-time reverse transcription-PCR and western blot assay were applied to detect mRNA and protein expression of intelectin-2 and nuclear factor-kappa B in the viral encephalitis and control groups. Nuclear factor-kappa B and intelectin-2 mRNA and protein expression were significantly increased in mice with viral encephalitis. After intraperitoneal injection of Shuanghuanglian at a dose of 1.5 mg/kg for 5 successive days, intelectin-2 and nuclear factor-kappa B protein and mRNA expression were significantly decreased. To elucidate the relationship between intelectin-2 and nuclear factor-kappa B, mice with viral encephalitis were administered an intracerebral injection of 107 pfu recombinant lentivirus expressing intelectin shRNA. Both protein and mRNA levels of intelectin and nuclear factor-kappa B in brain tissue of mice were significantly decreased. Experimental findings suggest that Shuanghuanglian injection may downregulate nuclear factor-kappa B production via suppression of intelectin production, thus inhibiting inflammation associated with viral encephalitis. 展开更多
关键词 intelectin nuclear factor-kappa b viral encephalitis short hairpin RNA Shuanghuanglian injection mice lentivirus nervous system disease traditional Chinese medicine neural regeneration
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Effects of Five Chitosan Oligosaccharides on Nuclear Factor-kappa B Signaling Pathway
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作者 李贤 周长忍 《Journal of Wuhan University of Technology(Materials Science)》 SCIE EI CAS 2012年第2期276-279,共4页
The effects of five chito-oligomers, from dimer to hexamer (chitobiose, chitotriose, chitotetraose, chitopentaose, chitohexaose) separated from chitosan oligosaccharides, on nuclear factor -kappaB (NF-rd3) signali... The effects of five chito-oligomers, from dimer to hexamer (chitobiose, chitotriose, chitotetraose, chitopentaose, chitohexaose) separated from chitosan oligosaccharides, on nuclear factor -kappaB (NF-rd3) signaling pathway were investigated by using luciferase assay and laser scanning microscopy. The expression of NF-rd3 downstream genes (cyclin DI, TNFa and IL-6) were tested by real time PCR. We found that all five chitosan oligosaccharides increased NF-KB-dependent luciferase gene expression and NF-KB downstream genes transcription, and the most significant were chitotetraose and chitohexaose. In addition, laser scanning microscopy experiments showed that chitotetraose and chitohexaose also activated the p65 subunite of NF-kB translocating from cytoplasm to nucleus, which suggested that they were the most potent activators of NF-kB signaling pathway. 展开更多
关键词 CHITOSAN chitosan oligosaccharide nuclear factor-kappa b inflammatory response
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Effects of transplantation of microencapsulated rabbit sciatic nerve on nuclear factor-kappa B expression after spinal cord injury in rats
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作者 Xiaolian Wang Jianmin Ma Hui Chen Deming Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2009年第3期213-217,共5页
BACKGROUND: It has been reported that nuclear factor-kappa B (NF- κB), activated after spinal cord injury in rats, plays a key role in inflammatory responses in the central nervous system. OBJECTIVE: To investiga... BACKGROUND: It has been reported that nuclear factor-kappa B (NF- κB), activated after spinal cord injury in rats, plays a key role in inflammatory responses in the central nervous system. OBJECTIVE: To investigate the effects of transplantation of microencapsulated rabbit sciatic nerve on NF- κB expression and motor function after spinal cord injury in rats, and to compare the results with the transplantation of rabbit sciatic nerve alone. DESIGN, TIME AND SETTING: This completely randomized, controlled study was performed at the Department of Neurobiology, Medical College of Nanchang University between December 2007 and July 2008. MATERIALS: A rabbit anti-NF- κB P65 monoclonal antibody was made by the Santa Cruz Company, USA and a streptavidin peroxidase immunohistochemical kit was provided by the Sequoia Company, China. METHODS: Eight rabbits were used to prepare a sciatic nerve cell suspension that was divided into two parts: one stored for transplantation, and the other mixed with a 1.5% sodium alginate solution. One hundred and twenty adult Sprague Dawley rats weighing 220-250 g were randomly divided into four groups: the microencapsulated cell group (n = 36), the non-encapsulated cell group (n = 36), the saline group (n = 36) and the sham operation group (n = 12). The first three groups underwent a right hemisection injury of the spinal cord at the T10 level, into which was transplanted a gelatin sponge soaked with 10 μL of a microencapsulated nerve tissue/cell suspension (microencapsulated cell group), a tissue/cell suspension (non-encapsulated cell group) or physiological saline (saline group). In the sham operation group the vertebrae were exposed, but the spinal cord was not injured, and no implantation was given. MAIN OUTCOME MEASURES: Pathological changes were detected using hematoxylin-eosin staining; NF- κB expression was quantified using immunohistochemical staining; motor function was assessed using the Basso, Beattie and Bresnahan (BBB) scale. RESULTS: Spinal cord injuries, such as neuronal death and inflammatory cell infiltration, were found in the microencapsulated cell group, the non-encapsulated cell group and the saline group. However, the damage in the microencapsulated cell group was milder than in the non-encapsulated cell or saline groups. NF- κB expression in the microencapsulated cell group, the non-encapsulated cell group and the saline group was increased after spinal cord injury; it reached a peak after 24 hours, gradually decreased after 3 days, and was close to normal levels after 7 days. NF- κB expression in the microencapsulated cell group was significantly lower than in the saline group and the non-encapsulated cell group (P 〈 0.05). With time, the motor function of the animals in each group improved to a certain extent, but did not reach normal levels. There were no significant differences in BBB scores between the different groups on post-operative day 3; however, the BBB scores for the microencapsulated cell group and the non-encapsulated cell group were significantly higher than the saline group on post-operative day 7 (P 〈 0.05). In addition, the motor function recovered better in the microencapsulated cell group than in the non-encapsulated cell group (P 〈 0.05). CONCLUSION: The transplantation of microencapsulated rabbit sciatic nerve can inhibit NF- κB expression and inflammatory reactions and promote recovery of motor function after spinal cord injury in rats. The effects of microencapsulated cell transplantation are superior to those of transplantation of cells alone. 展开更多
关键词 microcaosule: soinal cord iniurv: transolantation: nuclear factor-kappa b
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Inhibitory effects of saikosaponin-d on CCl_4-induced hepatic fibrogenesis in rats 被引量:41
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作者 Shuang-Suo Dang Bao-Feng Wang +3 位作者 Yan-An Cheng Ping Song Zhen-Guo Liu Zong-Fang Li 《World Journal of Gastroenterology》 SCIE CAS CSCD 2007年第4期557-563,共7页
AIM: To investigate the suppressive effect of saikosaponin-d (SSd) on hepatic fibrosis in rats induced by CCh injections in combination with alcohol and high fat, low protein feeding and its relationship with the e... AIM: To investigate the suppressive effect of saikosaponin-d (SSd) on hepatic fibrosis in rats induced by CCh injections in combination with alcohol and high fat, low protein feeding and its relationship with the expression of nuclear factor-κB (NF-κB), tumor necrosis factor-alpha (TNF-α) and interleukins-6 (IL-6). METHODS: Hepatic fibrosis models were induced by subcutaneous injection of CCh at a dosage of 3 mL/kg in rats. At the same time, rats in treatment groups were injected intraperitoneally with SSd at different doses (1.0, 1.5 and 2.0 mg/kg) once daily for 6 wk in combination with CCh, while the control group received olive oil instead of CCh. At the end of the experiment, rats were anesthetized and killed (except for 8 rats which died during the experiment; 2 from the model group, 3 in high-dose group, 1 in medium-dose group and 2 in lowdose group). Hernatoxylin and eosin (HE) staining and Van Gieson staining were used to examine the changes in liver pathology. The levels of alanine aminotransferase (ALT), triglyeride (TG), albumin (ALB), globulin (GLB), hyaluronic acid (HA) and larninin (LN) in serum and the content of hydroxyproline (HYP) in liver were measured by biochemical examinations and radioimmuneoassay, respectively. In addition, the expression of TNF-α and IL-6 in liver homogenate was evaluated by enzymelinked immunosorbent assay (ELISA) and the levels of NF-κBp65 and I-κBa in liver tissue were analyzed by Western blotting. RESULTS: Both histological examination and Van Gieson staining demonstrated that SSd could attenuate the area and extent of necrosis and reduce the scores of liver fibrosis. Similarly, the levels of ALT, TG, GLB, HA, and LN in serum, and the contents of HYP, TNF-α and IL-6 in liver were all significantly increased in model group in comparison with those in control group. Whereas, the treatment with SScl markedly reduced all the above parameters compared with the model group, especially in the medium group (ALT: 412 ± 94.5 IU/L vs 113.76 ± 14.91 IU/L, TG: 0.95 ± 0.16 mmol/L vs 0.51 ± 0.06 mmol/L, GLB: 35.62 ± 3.28 g/L vs 24.82 ± 2.73 g/L, HA: 42.15 ± 8.25 ng/mL vs 19.83 ± 3.12 ng/mL, LN: 27.56 ± 4.21 ng/mL vs 13.78 ± 2.57 ng/mL, HYP: 27.32 ± 4.32 ug/mg vs 16.20 ± 3.12 ug/mg, TNF-a: 4.38 ± 0.76 ng/L vs 1.94 ± 0.27 ng/L, IL-6:28.24 ± 6.37 pg/g vs 12.72 ± 5.26 pg/g, respectively, P 〈 0.01). SSd also decreased ALB in serum (28.49 ± 4.93 g/L vs 37.51 ± 3.17 g/L, P 〈 0.05). Moreover, the expression of NF-KB p65 in the liver of treated groups was lower than that in model groups while the expression of I-κBa was higher in treated group than in model group (P 〈 0.01). The expression of NF-κBp65 and TNF-a had a positive correlation with the level of HA in serum of rats after treatment with CCh (r = 0.862, P 〈 0.01; r = 0.928, P 〈 0.01, respectively). CONCLUSION: SSd attenuates CCh-induced hepatic fibrosis in rats, which may be related to its effects of hepato-protective and anti-inflammation properties, the down-regulation of liver TNF-a, IL-6 and NF-κBp65 expression and the increased I-κBa activity in liver. 展开更多
关键词 Saikosaponin-d Hepatic fibrosis Tumornecrosis factor Interleukins-6 nuclear factor-Kb inhibitory κb alpha
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EFFECT OF OXIDIZED-LDL ON NF-κB NUCLEAR TRANSLOCATION IN AORTIC SMOOTH MUSCLE CELLS ORIGINATED FROM RATS OF DIFFERENT AGES 被引量:2
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作者 Jun-huaZhang LiZhou Hong-chaoYin Pei-maoLiu HuaZhang Ming-pengShe 《Chinese Medical Sciences Journal》 CAS CSCD 2005年第2期112-115,共4页
Objective To investigate the molecular mechanism of atherosclerosis that related to age. Methods Immunohistochemistry staining and Western blot were adopted to determine the nuclear translocation of nuclear factor-kap... Objective To investigate the molecular mechanism of atherosclerosis that related to age. Methods Immunohistochemistry staining and Western blot were adopted to determine the nuclear translocation of nuclear factor-kappa B (NF-κB) and expression of platelet-derived growth factor B (PDGF-B) in smooth muscle cells (SMCs) co-cultured with low density lipoprotein (LDL), oxidized LDL (ox-LDL), and ox-LDL+high density lipoprotein (HDL) originated from rats of 2 and 10 months old respectively. Fat stain was used to identify the lipid intake in SMCs. Results The optimal stimulation time of ox-LDL to SMCs was 12 hours. NF-κB intensity increased in most nuclei of SMCs that originated from rats of either 2 or 10 months old co-cultured with ox-LDL. The intensity of NF-κB and the amount of intracellular lipid taken in SMCs were more obvious in cells from 10-month-old rats than from the younger ones. Change of PDGF-B expression in SMCs was not remarkable in each group of rats. Conclusions The 10-month-old rats are more susceptive to ox-LDL than 2-month-old rats in activating nuclear transloca- tion of NF-κB. Maybe this is one of the important reasons contributing to the difference between the older and younger rats on the initiation and development of atherosclerosis lesion. Expression of PDGF-B is not associated with the activity of nuclear translocation of NF-κB. 展开更多
关键词 oxidized low density lipoprotein nuclear factor-kappa b platelet-derived growth factor b smooth muscle cell
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Ketogenic diet alleviates cognitive dysfunction and neuroinflammation in APP/PS1 mice via the Nrf2/HO-1 and NF-κB signaling pathways 被引量:1
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作者 Jingwen Jiang Hong Pan +2 位作者 Fanxia Shen Yuyan Tan Shengdi Chen 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第12期2767-2772,共6页
Alzheimer's disease is a progressive neurological disorder characterized by cognitive decline and chronic inflammation within the brain.The ketogenic diet,a widely recognized therapeutic intervention for refractor... Alzheimer's disease is a progressive neurological disorder characterized by cognitive decline and chronic inflammation within the brain.The ketogenic diet,a widely recognized therapeutic intervention for refractory epilepsy,has recently been proposed as a potential treatment for a variety of neurological diseases,including Alzheimer's disease.However,the efficacy of ketogenic diet in treating Alzheimer's disease and the underlying mechanism remains unclear.The current investigation aimed to explore the effect of ketogenic diet on cognitive function and the underlying biological mechanisms in a mouse model of Alzheimer's disease.Male amyloid precursor protein/presenilin 1(APP/PS1)mice were randomly assigned to either a ketogenic diet or control diet group,and received their respective diets for a duration of 3 months.The findings show that ketogenic diet administration enhanced cognitive function,attenuated amyloid plaque formation and proinflammatory cytokine levels in APP/PS1 mice,and augmented the nuclear factor-erythroid 2-p45 derived factor 2/heme oxygenase-1 signaling pathway while suppressing the nuclear factor-kappa B pathway.Collectively,these data suggest that ketogenic diet may have a therapeutic potential in treating Alzheimer's disease by ameliorating the neurotoxicity associated with Aβ-induced inflammation.This study highlights the urgent need for further research into the use of ketogenic diet as a potential therapy for Alzheimer's disease. 展开更多
关键词 Alzheimer's disease APP/PS1 mice cognitive impairment ketogenic diet NEUROINFLAMMATION nuclear factor-kappa b pathway nuclear factor-erythroid 2-p45 derived factor 2/heme oxygenase-1 therapeutic benefits
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Salvianic acid A inhibits induction of inflammatory mediators by blocking Nuclear Factor-κB activation in macrophages
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作者 YUAN Jun,YAO Ji-hong,ZHOU Qin(Dalian Medical University,Dalian 116044,China) 《沈阳药科大学学报》 CAS CSCD 北大核心 2008年第S1期104-105,共2页
Objective To investigate the anti-inflammation effect and possible mechanism of Salvianic acid A(SAA)in mouse peritoneal macrophages.Methods Peritoneal macrophages were obtained from BALB/c mice.LPS induced nitric oxi... Objective To investigate the anti-inflammation effect and possible mechanism of Salvianic acid A(SAA)in mouse peritoneal macrophages.Methods Peritoneal macrophages were obtained from BALB/c mice.LPS induced nitric oxide(NO),tumor necrosis factor-alpha(TNF-α)and interleukin-6(IL-6)in supernatant,protein expression of inducible nitric oxide synthase(iNOS),matrix metalloproteinase-9(MMP-9)and activation of nuclear factor-kappa B(NF-κB)in the extract were measured.Results SAA strongly inhibited the excessive production of NO,TNF-α and IL-6 in LPS-induced peritoneal macrophages in a concentration-dependent manner and blocked the expression of iNOS and MMP-9.Treatment with LPS alone increased the translocation of NF-κB(p65)from cytosol to the nucleus,but the SAA inhibited the translocation of NF-κB(p65).Conclusions The results showed that SAA had strong anti-inflammatory effects in LPS-stimulated peritoneal macrophages.The important mechanism is due to its inhibition of NF-κB activation. 展开更多
关键词 salvianic ACID a tumor NECROSIS factor-α nterleukin-6 INDUCIbLE NITRIC oxide SYNTHASE matrix metalloproteinase-9 nuclear factor-kappa b
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L-and T-type Ca^(2+)channels dichotomously contribute to retinal ganglion cell injury in experimental glaucoma
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作者 Hong-Ning Wang Wen-Jing Qian +5 位作者 Guo-Li Zhao Fang Li Yan-Ying Miao Bo Lei Xing-Huai Sun Zhong-Feng Wang 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第7期1570-1577,共8页
Retinal ganglion cell apoptotic death is the main pathological characteristic of glaucoma,which is the leading cause of irreversible blindness.Disruption of Ca^(2+)homeostasis plays an important role in glaucoma.Volta... Retinal ganglion cell apoptotic death is the main pathological characteristic of glaucoma,which is the leading cause of irreversible blindness.Disruption of Ca^(2+)homeostasis plays an important role in glaucoma.Voltage-gated Ca^(2+)channel blockers have been shown to improve vision in patients with glaucoma.However,whether and how voltage-gated Ca^(2+)channels are involved in retinal ganglion cell apoptotic death are largely unknown.In this study,we found that total Ca^(2+)current densities in retinal ganglion cells were reduced in a rat model of chronic ocular hypertension experimental glaucoma,as determined by whole-cell patch-clamp electrophysiological recordings.Further analysis showed that L-type Ca^(2+)currents were downregulated while T-type Ca^(2+)currents were upregulated at the later stage of glaucoma.Western blot assay and immunofluorescence experiments confirmed that expression of the Ca_(V)1.2 subunit of L-type Ca^(2+)channels was reduced and expression of the Ca_(V)3.3 subunit of T-type Ca^(2+)channels was increased in retinas of the chronic ocular hypertension model.Soluble tumor necrosis factor-α,an important inflammatory factor,inhibited the L-type Ca^(2+)current of isolated retinal ganglion cells from control rats and enhanced the T-type Ca^(2+)current.These changes were blocked by the tumor necrosis factor-αinhibitor XPro1595,indicating that both types of Ca^(2+)currents may be mediated by soluble tumor necrosis factor-α.The intracellular mitogen-activated protein kinase/extracellular signal-regulated kinase pathway and nuclear factor kappa-B signaling pathway mediate the effects of tumor necrosis factor-α.TUNEL assays revealed that mibefradil,a T-type calcium channel blocker,reduced the number of apoptotic retinal ganglion cells in the rat model of chronic ocular hypertension.These results suggest that T-type Ca^(2+)channels are involved in disrupted Ca^(2+)homeostasis and apoptosis of retinal ganglion cells in glaucoma,and application of T-type Ca^(2+)channel blockers,especially a specific CaV3.3 blocker,may be a potential strategy for the treatment of glaucoma. 展开更多
关键词 apoptosis CaV1.2 CaV3.3 chronic ocular hypertension extracellular signal-regulated kinase mitogen-activated protein kinase nuclear factor-kappa b PATCH-CLAMP RETINA tumor necrosis factor-α
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siRNA阻断NF-κB信号通路抑制胃癌SGC-7901细胞的增殖及侵袭 被引量:3
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作者 王红军 廖新华 +1 位作者 崔飞博 魏光兵 《西安交通大学学报(医学版)》 CAS CSCD 北大核心 2012年第4期466-469,共4页
目的采用RNA干扰(RNA interference,RNAi)技术下调胃癌细胞株SGC-7901中NF-κB p65基因的表达,探讨其对肿瘤细胞增殖活性和侵袭能力的影响。方法利用阳离子脂质体LipofectamineTM2000将化学合成的人NF-κB p65的小干扰RNA(small interfe... 目的采用RNA干扰(RNA interference,RNAi)技术下调胃癌细胞株SGC-7901中NF-κB p65基因的表达,探讨其对肿瘤细胞增殖活性和侵袭能力的影响。方法利用阳离子脂质体LipofectamineTM2000将化学合成的人NF-κB p65的小干扰RNA(small interference RNA,siRNA)转染入胃癌细胞株SGC-7901中。采用RT-PCR法测定细胞内NF-κB p65mRNA的表达;酶联免疫吸附测定法(ELISA)检测NF-κB亚单位p65的DNA结合活性的改变;采用MTT法测定细胞增殖活性的变化;利用Transwell侵袭实验检测细胞体外侵袭能力的变化。结果与对照组比较,化学合成的人NF-κB p65siRNA能有效地抑制SGC-7901细胞中NF-κB p65mRNA的表达(P<0.05);RelAsiRNA组的p65亚单位与DNA结合活性明显低于对照组(P<0.05),并且RelA siRNA组中SGC-7901细胞的体外侵袭力减弱,增殖活性降低。结论特异的siRNA可以有效阻断NF-κB信号通路,影响人胃癌细胞的增殖活性和体外侵袭能力。 展开更多
关键词 胃癌 nuclear factor-kappa b(NF-κb) RNA干扰 细胞侵袭 细胞增殖
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NF-κB信号转导通路与胰岛素抵抗 被引量:10
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作者 金华 陈名道 杨颖 《上海交通大学学报(医学版)》 CAS CSCD 北大核心 2009年第4期461-464,共4页
核因子-κB(NF-κB)信号转导通路包括NF-κB、NF-κB抑制蛋白(IκB)和IκB激酶(IKK)。其中,NF-κB是一种重要的核转录因子,参与炎症反应、免疫反应、细胞凋亡及物质代谢等多种生物进程。IKK具有丝氨酸/苏氨酸激酶活性,能使多种蛋白的丝... 核因子-κB(NF-κB)信号转导通路包括NF-κB、NF-κB抑制蛋白(IκB)和IκB激酶(IKK)。其中,NF-κB是一种重要的核转录因子,参与炎症反应、免疫反应、细胞凋亡及物质代谢等多种生物进程。IKK具有丝氨酸/苏氨酸激酶活性,能使多种蛋白的丝氨酸/苏氨酸残基磷酸化。NF-κB信号转导通路的活化与胰岛素抵抗的发生密切相关。文章就NF-κB在胰岛素抵抗发生中作用作一综述。 展开更多
关键词 核因子-Κb 核因子-κb抑制蛋白 核因子-κb抑制蛋白激酶 胰岛素抵抗
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小剂量氢化可的松对脓毒症大鼠海马组织核因子κB表达的影响 被引量:8
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作者 武志远 曾建生 樊寻梅 《实用儿科临床杂志》 CAS CSCD 北大核心 2006年第6期331-333,共3页
目的研究小剂量氢化可的松(HC)对内毒素诱导的脓毒症大鼠海马组织核因子-κB(NF-κB)、抑制因子κB(IκB)表达的影响。方法雄性Wistar大鼠54只随机分为:对照组(A组)6只,模型组(B组)24只、小剂量HC干预组(C组)24只。腹腔注射脂多糖(LPS)1... 目的研究小剂量氢化可的松(HC)对内毒素诱导的脓毒症大鼠海马组织核因子-κB(NF-κB)、抑制因子κB(IκB)表达的影响。方法雄性Wistar大鼠54只随机分为:对照组(A组)6只,模型组(B组)24只、小剂量HC干预组(C组)24只。腹腔注射脂多糖(LPS)1 mg/kg建立脓毒症大鼠模型,尾静脉注射小剂量HC(6 mg/kg)作为干预,分别在注射后2、8、16、24 h分时段麻醉并灌注固定取脑。B组和C组每个时段点各6只。采用免疫组织化学方法及医学图像分析系统检测大鼠海马NF-κBI、κB的表达。结果模型组NF-κB表达较正常对照组显著上调(P<0.05),IκB表达先降低后逐步上升,较对照组亦明显增加(P<0.05),以8 h为最高;干预组海马NF-κB表达较模型组显著下调(P<0.05);IκB表达较模型组明显增加(P<0.05)。结论小剂量HC可通过诱生IκB来抑制NF-κB的表达,进而调控LPS诱导的脓毒症脑功能障碍,NF-κB信号转导途径在其发病机制中起重要作用。 展开更多
关键词 核因子 Kb 抑制因子 氢化可的松 内毒素 脓毒症 海马
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金雀异黄素抑制人血管平滑肌细胞中核因子κB的激活 被引量:5
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作者 冯赞杰 卢志顺 +2 位作者 刘洋 李琴山 钱民章 《中国动脉硬化杂志》 CAS CSCD 北大核心 2009年第5期363-366,共4页
目的研究金雀异黄素对氧化型低密度脂蛋白诱导的人血管平滑肌细胞中核因子κB激活的影响,并对其作用机制进行初步探讨。方法以体外培养的人脐静脉平滑肌细胞为对象,用50 mg/L的氧化型低密度脂蛋白作用细胞2 h,并加入不同浓度金雀异黄素(... 目的研究金雀异黄素对氧化型低密度脂蛋白诱导的人血管平滑肌细胞中核因子κB激活的影响,并对其作用机制进行初步探讨。方法以体外培养的人脐静脉平滑肌细胞为对象,用50 mg/L的氧化型低密度脂蛋白作用细胞2 h,并加入不同浓度金雀异黄素(10,30,90 mol/L)对其进行干预,免疫细胞化学方法检测各组血管平滑肌细胞中核因子κB亚单位p65核移位阳性细胞数,Western blot法检测细胞内κB抑制蛋白-α含量变化,硝酸还原酶法测定各组细胞培养液中一氧化氮生成量。结果人脐静脉平滑肌细胞经氧化型低密度脂蛋白刺激2 h后,其核移位阳性细胞数为76.67±3.21,与空白组1.33±0.58相比明显增加(P<0.01),再与不同浓度金雀异黄素共同孵育2 h后,核移位阳性细胞数分别为28.33±2.52,19.67±1.53和15.67±2.89,与单纯给予氧化型低密度脂蛋白刺激相比明显减少(P<0.01),且随着浓度升高有递减的趋势;30,90μmol/L金雀异黄素能明显增加细胞内κB抑制蛋白-α的含量;各组细胞培养液内的一氧化氮生成量差异无显著性。结论金雀异黄素能抑制氧化型低密度脂蛋白诱导的血管平滑肌细胞中核因子κB的活化;其作用机制可能涉及增加细胞内κB抑制蛋白含量,未发现与一氧化氮有关。 展开更多
关键词 金雀异黄素 核因子Κb 氧化型低密度脂蛋白 κb抑制蛋白-α 动脉粥样硬化
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