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Nitrite-derived nitric oxide by xanthine oxidoreductase protects the liver against ischemia- reperfusion injury 被引量:4
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作者 Department of General Surgery ( Lu P, Wang CY and Chen DD), and Department of Radiology (Liu F), Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China Cold Spring Harbor Laboratory, New York 11724, USA ( Yao Z) General Surgery Laboratory, Union Hospital, Tongji Medical College , Huazhong University of Science and Technology, Wuhan 430022 , China (Tian Y, Zhang JH and Wu YH) 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2005年第3期350-355,共6页
It was demonstrated that xanthine oxidoreductase (XOR), during ischemia, catalyzes the formation of nitric oxide (NO) from nitrite (NO_2^-) and this NO_2^--derived NO protects the isolated perfused rat heart against t... It was demonstrated that xanthine oxidoreductase (XOR), during ischemia, catalyzes the formation of nitric oxide (NO) from nitrite (NO_2^-) and this NO_2^--derived NO protects the isolated perfused rat heart against the damaging effects of ischemia-reperfusion (I/R) when conventional nitric oxide synthase (NOS) -dependent NO production is impaired. Liver is one of the organs with the highest XOR concentration. This study was designed to determine whether NO_2^--derived NO by XOR protects liver against I/R injury in vivo. For its minute amounts and active reactivity, NO can not be detected directly in real time in vivo by this time. We have to prove the above hypothesis indirectly. METHODS:Wistar rats were pretreated with saline, NOS inhibitor L-NAME (10 mg/kg intravenously), XOR inhibitor allopurinol (1.5 mg/kg orally), L-NAME +allopurinol and NO scavenger carboxy-PTIO (0.6 mg/kg intravenously) respectively (12 animals per group). And then, they were subjected to total liver ischemia for 40 minutes followed by reperfusion. Blood samples and liver tissues were obtained for analysis after 3 hours of reperfusion. Survival was also investigated. RESULTS:Allopurinol-treated animals exhibited further increased serum alanine aminotransferase (ALT) levels and liver myeloperoxidase (MPO) activities, but further decreased liver adenosine triphosphate (ATP) stores after I/R compared to saline-treated counterparts (830.5±108.3 U/L, 56.5±11.0 U/mg protein and 1.93±0.47 μmol/g vs. 505.8± 184.2 U/L, 41.5±10.2 U/mg protein and 3.05±0.55 μmol/g respectively, P<0.01, P<0.05 and P<0.01 respectively). The hepatocyte injury was further exacerbated and the overall survival rate was significantly decreased after I/R in animals given by allopurinol compared to those pretreated by saline (P<0.05). L-NAME and allopurinol co-treated animals exhibited more severe liver injury (P<0.05 and P<0.01) and a further decreased overall survival rate (P<0.05) compared to L-NAME or allopurinol alone-treated counterparts, but they were not different from carboxy-PTIO treated animals (P>0.05). CONCLUSION:NO_2^--derived NO by XOR in the hypoxic and acidic environment induced by hepatic I/R protects the liver against I/R injury in vivo. 展开更多
关键词 NITRITES nitric oxide ischemia-reperfusion injury
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Neuroprotective potential for mitigating ischemia-reperfusion-induced damage
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作者 Zi Ye Runqing Liu +6 位作者 Hangxing Wang Aizhen Zuo Cen Jin Nan Wang Huiqi Sun Luqian Feng Hua Yang 《Neural Regeneration Research》 SCIE CAS 2025年第8期2199-2217,共19页
Reperfusion following cerebral ischemia causes both structural and functional damage to brain tissue and could aggravate a patient's condition;this phenomenon is known as cerebral ischemia-reperfusion injury.Curre... Reperfusion following cerebral ischemia causes both structural and functional damage to brain tissue and could aggravate a patient's condition;this phenomenon is known as cerebral ischemia-reperfusion injury.Current studies have elucidated the neuroprotective role of the sirtuin protein family(Sirtuins)in modulating cerebral ischemia-reperfusion injury.However,the potential of utilizing it as a novel intervention target to influence the prognosis of cerebral ischemia-reperfusion injury requires additional exploration.In this review,the origin and research progress of Sirtuins are summarized,suggesting the involvement of Sirtuins in diverse mechanisms that affect cerebral ischemia-reperfusion injury,including inflammation,oxidative stress,blood-brain barrier damage,apoptosis,pyroptosis,and autophagy.The therapeutic avenues related to Sirtuins that may improve the prognosis of cerebral ischemia-reperfusion injury were also investigated by modulating Sirtuins expression and affecting representative pathways,such as nuclear factor-kappa B signaling,oxidative stress mediated by adenosine monophosphate-activated protein kinase,and the forkhead box O.This review also summarizes the potential of endogenous substances,such as RNA and hormones,drugs,dietary supplements,and emerging therapies that regulate Sirtuins expression.This review also reveals that regulating Sirtuins mitigates cerebral ischemia-reperfusion injury when combined with other risk factors.While Sirtuins show promise as a potential target for the treatment of cerebral ischemiareperfusion injury,most recent studies are based on rodent models with circadian rhythms that are distinct from those of humans,potentially influencing the efficacy of Sirtuinstargeting drug therapies.Overall,this review provides new insights into the role of Sirtuins in the pathology and treatment of cerebral ischemia-reperfusion injury. 展开更多
关键词 apoptosis autophagy blood-brain barrier dietary supplements drug HORMONES inflammation NEUROPROTECTION oxidative stress prognosis PYROPTOSIS reperfusion injury risk factors RNA THERAPEUTICS
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Endoplasmic reticulum stress and autophagy in cerebral ischemia/reperfusion injury:PERK as a potential target for intervention
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作者 Ju Zheng Yixin Li +8 位作者 Ting Zhang Yanlin Fu Peiyan Long Xiao Gao Zhengwei Wang Zhizhong Guan Xiaolan Qi Wei Hong Yan Xiao 《Neural Regeneration Research》 SCIE CAS 2025年第5期1455-1466,共12页
Several studies have shown that activation of unfolded protein response and endoplasmic reticulum(ER)stress plays a crucial role in severe cerebral ischemia/reperfusion injury.Autophagy occurs within hours after cereb... Several studies have shown that activation of unfolded protein response and endoplasmic reticulum(ER)stress plays a crucial role in severe cerebral ischemia/reperfusion injury.Autophagy occurs within hours after cerebral ischemia,but the relationship between ER stress and autophagy remains unclear.In this study,we established experimental models using oxygen-glucose deprivation/reoxygenation in PC12 cells and primary neurons to simulate cerebral ischemia/reperfusion injury.We found that prolongation of oxygen-glucose deprivation activated the ER stress pathway protein kinase-like endoplasmic reticulum kinase(PERK)/eukaryotic translation initiation factor 2 subunit alpha(e IF2α)-activating transcription factor 4(ATF4)-C/EBP homologous protein(CHOP),increased neuronal apoptosis,and induced autophagy.Furthermore,inhibition of ER stress using inhibitors or by si RNA knockdown of the PERK gene significantly attenuated excessive autophagy and neuronal apoptosis,indicating an interaction between autophagy and ER stress and suggesting PERK as an essential target for regulating autophagy.Blocking autophagy with chloroquine exacerbated ER stress-induced apoptosis,indicating that normal levels of autophagy play a protective role in neuronal injury following cerebral ischemia/reperfusion injury.Findings from this study indicate that cerebral ischemia/reperfusion injury can trigger neuronal ER stress and promote autophagy,and suggest that PERK is a possible target for inhibiting excessive autophagy in cerebral ischemia/reperfusion injury. 展开更多
关键词 APOPTOSIS ATF4 AUTOPHAGY C/EBP homologous protein cerebral ischemia/reperfusion injury EIF2Α endoplasmic reticulum stress PERK
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A matrix metalloproteinase-responsive hydrogel system controls angiogenic peptide release for repair of cerebral ischemia/reperfusion injury
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作者 Qi Liu Jianye Xie +5 位作者 Runxue Zhou Jin Deng Weihong Nie Shuwei Sun Haiping Wang Chunying Shi 《Neural Regeneration Research》 SCIE CAS 2025年第2期503-517,共15页
Vascular endothelial growth factor and its mimic peptide KLTWQELYQLKYKGI(QK)are widely used as the most potent angiogenic factors for the treatment of multiple ischemic diseases.However,conventional topical drug deliv... Vascular endothelial growth factor and its mimic peptide KLTWQELYQLKYKGI(QK)are widely used as the most potent angiogenic factors for the treatment of multiple ischemic diseases.However,conventional topical drug delivery often results in a burst release of the drug,leading to transient retention(inefficacy)and undesirable diffusion(toxicity)in vivo.Therefore,a drug delivery system that responds to changes in the microenvironment of tissue regeneration and controls vascular endothelial growth factor release is crucial to improve the treatment of ischemic stroke.Matrix metalloproteinase-2(MMP-2)is gradually upregulated after cerebral ischemia.Herein,vascular endothelial growth factor mimic peptide QK was self-assembled with MMP-2-cleaved peptide PLGLAG(TIMP)and customizable peptide amphiphilic(PA)molecules to construct nanofiber hydrogel PA-TIMP-QK.PA-TIMP-QK was found to control the delivery of QK by MMP-2 upregulation after cerebral ischemia/reperfusion and had a similar biological activity with vascular endothelial growth factor in vitro.The results indicated that PA-TIMP-QK promoted neuronal survival,restored local blood circulation,reduced blood-brain barrier permeability,and restored motor function.These findings suggest that the self-assembling nanofiber hydrogel PA-TIMP-QK may provide an intelligent drug delivery system that responds to the microenvironment and promotes regeneration and repair after cerebral ischemia/reperfusion injury. 展开更多
关键词 angiogenesis biomaterial blood-brain barrier cerebral ischemia/reperfusion injury control release drug delivery inflammation QK peptides matrix metalloproteinase-2 NEUROPROTECTION self-assembling nanofiber hydrogel
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N-acetylserotonin alleviates retinal ischemia-reperfusion injury via HMGB1/RAGE/NF-κB pathway in rats
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作者 Yu-Ze Zhao Xue-Ning Zhang +7 位作者 Yi Yin Pei-Lun Xiao Meng Gao Lu-Ming Zhang Shuan-Hu Zhou Shu-Na Yu Xiao-Li Wang Yan-Song Zhao 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2024年第2期228-238,共11页
AIM:To observe the effects of N-acetylserotonin(NAS)administration on retinal ischemia-reperfusion(RIR)injury in rats and explore the underlying mechanisms involving the high mobility group box 1(HMGB1)/receptor for a... AIM:To observe the effects of N-acetylserotonin(NAS)administration on retinal ischemia-reperfusion(RIR)injury in rats and explore the underlying mechanisms involving the high mobility group box 1(HMGB1)/receptor for advanced glycation end-products(RAGE)/nuclear factor-kappa B(NF-κB)signaling pathway.METHODS:A rat model of RIR was developed by increasing the pressure of the anterior chamber of the eye.Eighty male Sprague Dawley were randomly divided into five groups:sham group(n=8),RIR group(n=28),RIR+NAS group(n=28),RIR+FPS-ZM1 group(n=8)and RIR+NAS+FPS-ZM1 group(n=8).The therapeutic effects of NAS were examined by hematoxylin-eosin(H&E)staining,and retinal ganglion cells(RGCs)counting.The expression of interleukin 1 beta(IL-1β),HMGB1,RAGE,and nod-like receptor 3(NLRP3)proteins and the phosphorylation of nuclear factorkappa B(p-NF-κB)were analyzed by immunohistochemistry staining and Western blot analysis.The expression of HMGB1 protein was also detected by enzyme-linked immunosorbent assay(ELISA).RESULTS:H&E staining results showed that NAS significantly reduced retinal edema and increased the number of RGCs in RIR rats.With NAS therapy,the HMGB1 and RAGE expression decreased significantly,and the activation of the NF-κB/NLRP3 pathway was antagonized along with the inhibition of p-NF-κB and NLRP3 protein expression.Additionally,NAS exhibited an anti-inflammatory effect by reducing IL-1βexpression.The inhibitory of RAGE binding to HMGB1 by RAGE inhibitor FPS-ZM1 led to a significant decrease of p-NF-κB and NLRP3 expression,so as to the IL-1βexpression and retinal edema,accompanied by an increase of RGCs in RIR rats.CONCLUSION:NAS may exhibit a neuroprotective effect against RIR via the HMGB1/RAGE/NF-κB signaling pathway,which may be a useful therapeutic target for retinal disease. 展开更多
关键词 retinal diseases retinal ischemia—reperfusion injury N-ACETYLSEROTONIN high mobility group box 1 receptor for advanced glycation end-products nuclear factor-κB RATS
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Treatment with β-sitosterol ameliorates the effects of cerebral ischemia/reperfusion injury by suppressing cholesterol overload, endoplasmic reticulum stress, and apoptosis 被引量:4
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作者 Xiuling Tang Tao Yan +8 位作者 Saiying Wang Qingqing Liu Qi Yang Yongqiang Zhang Yujiao Li Yumei Wu Shuibing Liu Yulong Ma Le Yang 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第3期642-649,共8页
β-Sitosterol is a type of phytosterol that occurs naturally in plants.Previous studies have shown that it has anti-oxidant,anti-hyperlipidemic,anti-inflammatory,immunomodulatory,and anti-tumor effects,but it is unkno... β-Sitosterol is a type of phytosterol that occurs naturally in plants.Previous studies have shown that it has anti-oxidant,anti-hyperlipidemic,anti-inflammatory,immunomodulatory,and anti-tumor effects,but it is unknown whetherβ-sitosterol treatment reduces the effects of ischemic stroke.Here we found that,in a mouse model of ischemic stroke induced by middle cerebral artery occlusion,β-sitosterol reduced the volume of cerebral infarction and brain edema,reduced neuronal apoptosis in brain tissue,and alleviated neurological dysfunction;moreover,β-sitosterol increased the activity of oxygen-and glucose-deprived cerebral cortex neurons and reduced apoptosis.Further investigation showed that the neuroprotective effects ofβ-sitosterol may be related to inhibition of endoplasmic reticulum stress caused by intracellular cholesterol accumulation after ischemic stroke.In addition,β-sitosterol showed high affinity for NPC1L1,a key transporter of cholesterol,and antagonized its activity.In conclusion,β-sitosterol may help treat ischemic stroke by inhibiting neuronal intracellular cholesterol overload/endoplasmic reticulum stress/apoptosis signaling pathways. 展开更多
关键词 APOPTOSIS blood-brain barrier Β-SITOSTEROL cerebral ischemia/reperfusion injury cholesterol overload cholesterol transport endoplasmic reticulum stress ischemic stroke molecular docking NPC1L1
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The action mechanism by which C1q/tumor necrosis factor-related protein-6 alleviates cerebral ischemia/reperfusion injury in diabetic mice 被引量:2
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作者 Bo Zhao Mei Li +6 位作者 Bingyu Li Yanan Li Qianni Shen Jiabao Hou Yang Wu Lijuan Gu Wenwei Gao 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第9期2019-2026,共8页
Studies have shown that C1q/tumor necrosis factor-related protein-6 (CTRP6) can alleviate renal ischemia/reperfusion injury in mice. However, its role in the brain remains poorly understood. To investigate the role of... Studies have shown that C1q/tumor necrosis factor-related protein-6 (CTRP6) can alleviate renal ischemia/reperfusion injury in mice. However, its role in the brain remains poorly understood. To investigate the role of CTRP6 in cerebral ischemia/reperfusion injury associated with diabetes mellitus, a diabetes mellitus mouse model of cerebral ischemia/reperfusion injury was established by occlusion of the middle cerebral artery. To overexpress CTRP6 in the brain, an adeno-associated virus carrying CTRP6 was injected into the lateral ventricle. The result was that oxygen injury and inflammation in brain tissue were clearly attenuated, and the number of neurons was greatly reduced. In vitro experiments showed that CTRP6 knockout exacerbated oxidative damage, inflammatory reaction, and apoptosis in cerebral cortical neurons in high glucose hypoxia-simulated diabetic cerebral ischemia/reperfusion injury. CTRP6 overexpression enhanced the sirtuin-1 signaling pathway in diabetic brains after ischemia/reperfusion injury. To investigate the mechanism underlying these effects, we examined mice with depletion of brain tissue-specific sirtuin-1. CTRP6-like protection was achieved by activating the sirtuin-1 signaling pathway. Taken together, these results indicate that CTRP6 likely attenuates cerebral ischemia/reperfusion injury through activation of the sirtuin-1 signaling pathway. 展开更多
关键词 brain C1q/tumor necrosis factor-related protein-6 cerebral apoptosis diabetes inflammation ischemia/reperfusion injury NEURON NEUROPROTECTION oxidative damage Sirt1
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Homer1a reduces inflammatory response after retinal ischemia/reperfusion injury 被引量:1
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作者 Yanan Dou Xiaowei Fei +7 位作者 Xin He Yu Huan Jialiang Wei Xiuquan Wu Weihao Lyu Zhou Fei Xia Li Fei Fei 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第7期1608-1617,共10页
Elevated intraocular pressure(IOP)is one of the causes of retinal ischemia/reperfusion injury,which results in NRP3 inflammasome activation and leads to visual damage.Homerla is repo rted to play a protective role in ... Elevated intraocular pressure(IOP)is one of the causes of retinal ischemia/reperfusion injury,which results in NRP3 inflammasome activation and leads to visual damage.Homerla is repo rted to play a protective role in neuroinflammation in the cerebrum.However,the effects of Homerla on NLRP3inflammasomes in retinal ischemia/reperfusion injury caused by elevated IOP remain unknown.In our study,animal models we re constructed using C57BL/6J and Homer1^(flox/-)/Homerla^(+/-)/Nestin-Cre^(+/-)mice with elevated IOP-induced retinal ischemia/repe rfusion injury.For in vitro expe riments,the oxygen-glucose deprivation/repe rfusion injury model was constructed with M uller cells.We found that Homerla ove rexpression amelio rated the decreases in retinal thickness and Muller cell viability after ischemia/reperfusion injury.Furthermore,Homerla knockdown promoted NF-κB P65^(Ser536)activation via caspase-8,NF-κB P65 nuclear translocation,NLRP3 inflammasome formation,and the production and processing of interleukin-1βand inte rleukin-18.The opposite results we re observed with Homerla ove rexpression.Finally,the combined administration of Homerla protein and JSH-23 significantly inhibited the reduction in retinal thickness in Homer1^(flox/-)Homer1a^(+/-)/Nestin-Cre^(+/-)mice and apoptosis in M uller cells after ischemia/reperfusion injury.Taken together,these studies demonstrate that Homer1a exerts protective effects on retinal tissue and M uller cells via the caspase-8/NF-KB P65/NLRP3 pathway after I/R injury. 展开更多
关键词 CASPASE-8 Homer1a INTERLEUKIN-18 INTERLEUKIN-1Β intraocular pressure ischemia/reperfusion injury JSH-23 Müller cells NLRP3 nuclear factor-kB p65 RETINA
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Role of P-selectin and anti-P-selectin monoclonal antibody in apoptosis during hepatic/renal ischemia-reperfusion injury 被引量:10
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作者 Pei Wu Xiao Li +5 位作者 Tong Zhou Ming Jun Zhang Jin Lian Chen Wei Ming Wang Nan Chen De Chang Dong 《World Journal of Gastroenterology》 SCIE CAS CSCD 2000年第2期244-247,共4页
AIM To evaluale the potential role of P-selectinand anti-P-selectin monoclonal antibody(mAb)in apoptosis during hepatic/renal ischemia-reperfusion injury.METHODS Plasma P-selectin level,hepatic/renal P-selectin expres... AIM To evaluale the potential role of P-selectinand anti-P-selectin monoclonal antibody(mAb)in apoptosis during hepatic/renal ischemia-reperfusion injury.METHODS Plasma P-selectin level,hepatic/renal P-selectin expression and cell apoptosiswere detected in rat model of hepatic/ renalischemia-reperfusion injury.ELISA,immunohist-ochemistry and TUNEL were used.Someischemia-reperfusion rats were treated with anti-P-selectin mAb.RESULTS Hepatic/renal function insuffic-iency,up-regulated expression of P-selectin inplasma and hepatic/renal tissue,hepatic/renalhistopathological damages and cell apoptosiswere found in rats with hepatic/renal ischemia-reperfusion injury,while these changes becameless conspicuous in animals treated with anti-P-selectin mAb.CONCLUSION P-selectin might mediateneutrophil infiltration and cell apoptosis andcontribute to hepatic/renal ischemia-reperfusioninjury,anti-P-selectin mAb might be an efficientapproach for the prevention and treatment ofhepatic/renal ischemia-reperfusion injury. 展开更多
关键词 HEPATIC ISCHEMIA reperfusion injury renal ISCHEMIA reperfusion injury P-SELECTIN antibody monoclonal APOPTOSIS
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Plasma D(-)-lactate as a new marker for diagnosis of acute intestinal injury following ischemia-reperfusion 被引量:14
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作者 YAO YongMing1, YU Yan1, WU Ye2, LU LianRong1 and SHENG ZhiYong1 《World Journal of Gastroenterology》 SCIE CAS CSCD 1997年第4期27-29,共3页
IM To observe the kinetics of D()lactate alteration in both portal and systemic circulations, and its relationship with intestinal injury in rats subjected to acute intestinal ischemiareperfusion.METHODS Anesthetize... IM To observe the kinetics of D()lactate alteration in both portal and systemic circulations, and its relationship with intestinal injury in rats subjected to acute intestinal ischemiareperfusion.METHODS Anesthetized rats underwent 75min superior mesenteric artery occlusion followed by 6hour reperfusion. Plasma D()lactate levels were measured by an enzymatic spectrophotometric assay.RESULTS Intestinal ischemia for 75 min resulted in a significant elevation of D()lactate levels in portal vein as compared with the baseline values (P<005). Plasma D()lactate levels had a tendency to further increase after reperfusion up to 6 hours. Similar alterations in D()lactate were also found in systemic circulation, there were no significant differences between the portal and systemic circulations at any time point. Moreover, the macropathological evaluation scores were significantly correlated to the portal D()lactate levels in animals at various time points (r=0415, P<001). In addition,there was a remarkable rise of endotoxin concentration within the portal vein at the end of 75min ischemia (P<005), reaching a peak at 2 hours postreperfusion.CONCLUSION Acute intestinal ischemia is associated with failure of mucosal barrier resulting in increased plasma D()lactate levels in both portal and systemic blood. The subsequent reperfusion might further increase D()lactate levels, which are correlated to the macropathological alterations. Plasma D()lactate may be a useful marker of intestinal injury following both ischemia and reperfusion insults. 展开更多
关键词 D()lactate ENDOTOXIN INTESTINAL injury reperfusion injury
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Hepatic ischemia-reperfusion injury in liver transplant setting:mechanisms and protective strategies 被引量:17
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作者 Sanketh Rampes Daqing Ma 《The Journal of Biomedical Research》 CAS CSCD 2019年第4期221-234,共14页
Hepatic ischemia-reperfusion injury is a major cause of liver transplant failure,and is of increasing significance due to increased use of expanded criteria livers for transplantation.This review summarizes the mechan... Hepatic ischemia-reperfusion injury is a major cause of liver transplant failure,and is of increasing significance due to increased use of expanded criteria livers for transplantation.This review summarizes the mechanisms and protective strategies for hepatic ischemia-reperfusion injury in the context of liver transplantation.Pharmacological therapies,the use of pre-and post-conditioning and machine perfusion are discussed as protective strategies.The use of machine perfusion offers significant potential in the reconditioning of liver grafts and the prevention of hepatic ischemia-reperfusion injury,and is an exciting and active area of research,which needs more study clinically. 展开更多
关键词 liver TRANSPLANTATION reperfusion injury mechanism THERAPEUTICS ISCHEMIC PRECONDITIONING
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Effect of rosiglitazone on rabbit model of myocardial ischemia-reperfusion injury 被引量:5
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作者 Xia-Qing Gao Hua-Wei Li +3 位作者 Xue Ling Ya-Hui Qiu Yue Gao Yang Zhang 《Asian Pacific Journal of Tropical Medicine》 SCIE CAS 2013年第3期228-231,共4页
To explore mechanism and protective effect of rosiglitazone on myocardial ischemia reperfusion(I/R) injury.Methods:A total of 48 male Japanese white big-ear rabbits were randomly divided into control group(A),I/R grou... To explore mechanism and protective effect of rosiglitazone on myocardial ischemia reperfusion(I/R) injury.Methods:A total of 48 male Japanese white big-ear rabbits were randomly divided into control group(A),I/R group(B),low dose of rosiglitazone group(C),high dose of rosiglitazone group(D).Plasma concentration of and also reduced the concentration of plasma serum creatine kinase(CK),CK-MB.high-sensitivity C-reactive protein(hsCRP).ultrasuperoxide dismutase(SOD),malondialdehyde(MD.A).lactic acid glutathione skin peroxidase (C-SH-PX).nitric oxide(NO)and endothelin(ET) were measured 1 h later after I/R.Twenty-four hours after I/R the hearts were harvested for pathological and ultrastructural analysis.Area of myocardial infarction were tested.Results:Plasma concentration of CK,Ck-MB.hsCRP,NO. MDA and ET were decreased in C,D group compared with group B.Plasma concentration of T-SOD and GSH-Px were increased significantly in C.D group compared with group B.Compared with group B.pathological and ullraslructural changes in C and D group were slightly.There was significant difference in myocardial infarction area between group C.D and group B(P【0.05). Myocardial infarction area and arrhythmia rate were lower in group C,D compare with group B. Rosiglitazone may protect myocardium from I/R injury by enhancing T-SOD and GSH-Px concentration,inhibit inflammatory reaction,and improve endothelial function. 展开更多
关键词 ROSIGLITAZONE ISCHEMIA reperfusion injury MYOCARDIAL INFARCTION
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Monitoring somatosensory evoked potentials in spinal cord ischemia-reperfusion injury 被引量:7
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作者 Yiming Ji Bin Meng +2 位作者 Chenxi Yuan Huilin Yang Jun Zou 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第33期3087-3094,共8页
It remains unclear whether spinal cord ischemia-reperfusion injury caused by ischemia and other non-mechanical factors can be monitored by somatosensory evoked potentials. Therefore, we monitored spinal cord ischemia-... It remains unclear whether spinal cord ischemia-reperfusion injury caused by ischemia and other non-mechanical factors can be monitored by somatosensory evoked potentials. Therefore, we monitored spinal cord ischemia-reperfusion injury in rabbits using somatosensory evoked potential detection technology. The results showed that the somatosensory evoked potential latency was significantly prolonged and the amplitude significantly reduced until it disappeared during the period of spinal cord ischemia. After reperfusion for 30-180 minutes, the amplitude and latency began to gradually recover; at 360 minutes of reperfusion, the latency showed no significant difference compared with the pre-ischemic value, while the somatosensory evoked potential amplitude in- creased, and severe hindlimb motor dysfunctions were detected. Experimental findings suggest that changes in somatosensory evoked potentia~ ~atency can reflect the degree of spinat cord ischemic injury, while the amplitude variations are indicators of the late spinal cord reperfusion injury, which provide evidence for the assessment of limb motor function and avoid iatrogenic spinal cord injury. 展开更多
关键词 neural regeneration spinal cord injury somatosensory evoked potentials spinal cord ischemia reperfusion iatrogenic spinal cord injury HISTOPATHOLOGY abdominal aorta occlusion model latency grants-supported paper NEUROREGENERATION
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Protective effect of pyrrolidine dithiocarbamate on liver injury induced by intestinal ischemia-reperfusion in rats 被引量:10
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作者 Xiao-Feng Tian, Ji-Hong Yao, Ying-Hua Li, Hai-Feng Gao, Zhen-Zhen Wang, Chun-Ming Yang and Shu-Sen Zheng Department of General Surgery, Second Affiliated Hospital of Dalian Medical University, Dalian 116027, China Department of Pharmacology, Dalian Medical University, Dalian 116027, China and Department of Hepatobiliary and Pancreatic Surgery, First Affiliated Hospital, Zhejiang University School of Medicine. Hangzhou 310003, China 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2006年第1期90-95,共6页
BACKGROUND: The nuclear translocation of transcription factors may be a critical factor in the intracellular pathway involved in ischemia/reperfusion(I/R) injury. The aim of the study was to evaluate the role of nucle... BACKGROUND: The nuclear translocation of transcription factors may be a critical factor in the intracellular pathway involved in ischemia/reperfusion(I/R) injury. The aim of the study was to evaluate the role of nuclear factor-kappa B (NF-κB) in the pathogenesis of liver injury induced by intestinal ischemia/reperfusion (IIR) and to investigate the effect of pyrrolidine dithiocarbamate (PDTC) on this liver injury. METHODS: Male Wistar rats were divided randomly into three experimental groups (8 rats in each): sham operation group (control group); intestinal/reperfusion group(I/R group): animals received 1-hour of intestinal ischemia and 2-hour reperfusion; and PDTC treatment group (PDTC group): animals that received I/R subject to PDTC treatment (100 mg/kg). The histological changes in the liver and intestine were observed, and the serum levels of tumor necrosis factor-α (TNF-α), alanine aminotransferase (ALT), aspartate aminotransferase (AST), liver superoxide dismutase (SOD), and nitrite/nitrate (NO) were measured. The immunohistochemical expression and Western blot analysis of liver NF-κB and intercellular adhesion molecule-1(ICAM-1) were observed. RESULTS: IIR induced liver injury characterized by the histological changes of liver edema, hemorrhage, polymorphonuclear neutrophil (PMN) infiltration, and elevated serum levels of AST and ALT. The serum TNF-α level was significantly higher than that of the control group(P<0.01) and a high level of liver oxidant product was observed (P<0.01). These changes were parallel to the positive expression of NF-κB and ICAM-1. After the administration of PDTC, the histological changes after liver injury were improved; the levels of SOD and NO in the liver were elevated and reduced, respectively (P<0.01). The expressions of ICAM-1 and NF-κB in the liver were weakened (P<0.01). CONCLUSION: NF-κB plays an important role in the pathogenesis of liver injury induced by HR. PDTC, an agent known to inhibit the activation of NF-κB, can reduce and prevent this injury. 展开更多
关键词 liver injury intestinal ischemia/reperfusion nuclear factor kappa B pyrrolidine dithiocarbamate
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Attenuation of graft ischemia-reperfusion injury by urinary trypsin inhibitor in mouse intestinal transplantation 被引量:15
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作者 Ji-RenYu ShengYan Xiao-SunLiu Yi-JunWu Pei-FengFu Li-HuaWu Shu-SenZheng 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第11期1605-1609,共5页
AIM: Ischemia/reperfusion (I/R) injury is one of the major obstacles for intestinal transplantation (ITx). Urinary trypsin inhibitor (Ulinastatin, UTI) suppresses proteases and stabilizes lysosomal membranes. We suppo... AIM: Ischemia/reperfusion (I/R) injury is one of the major obstacles for intestinal transplantation (ITx). Urinary trypsin inhibitor (Ulinastatin, UTI) suppresses proteases and stabilizes lysosomal membranes. We supposed that Ulinastatin would diminish I/R injury of intestinal graft.METHODS: UTI- treated group and untreated control group were investigated by histological assessment at 1.5, 4, 24, and 72 h after ITx. Myeloperoxidase (MPO)activity was used as the activity of neutrophils, and malondialdehyde (MDA) was used as an index of lipid peroxidation. TNFα and i-NOS mRNA expression in graft tissue were measured by semi-quantitative RT-PCR.CD11b+ Gr1+ cells in graft lamina propria were analyzed by flow cytometry.RESULTS: Histological scores of the graft showed that the tissue injury was markedly attenuated by UTI treatment at different time points after ITx, with reduced MPO and MDA value in the grafts. The expression of TNFα and i-NOS mRNA was profoundly inhibited, while the infiltration of CD11b+ Gr1+ cells into the intestinal graft was decreased in UTI group.CONCLUSION: Urinary trypsin inhibitor attenuates I/R injury in mouse intestinal transplantation by reducing monocytes infiltration and down-regulation of TNFα and i-NOS mRNA expression. 展开更多
关键词 Ischemia/reperfusion injury ULINASTATIN Intestinal transplantation
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Fenofibrate Pre-treatment Suppressed Inflammation by Activating Phosphoinositide 3 Kinase/Protein Kinase B(PI3K/Akt) Signaling in Renal Ischemia-Reperfusion Injury 被引量:8
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作者 杨凤杰 何永华 周建华 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2015年第1期58-63,共6页
The aim of this study was to investigate the possible beneficial effects of Fenofibrate on renal ischemia-reperfusion injury(IRI) in mice and its potential mechanism. IRI was induced by bilateral renal ischemia for ... The aim of this study was to investigate the possible beneficial effects of Fenofibrate on renal ischemia-reperfusion injury(IRI) in mice and its potential mechanism. IRI was induced by bilateral renal ischemia for 60 min followed by reperfusion for 24 h. Eighteen male C57BL/6 mice were randomly divided into three groups: sham-operated group(sham), IRI+saline group(IRI group), IRI+Fenofibrate(FEN) group. Normal saline or Fenofibrate(3 mg/kg) was intravenously injected 60 min before renal ischemia in IRI group and FEN group, respectively. Blood samples and renal tissues were collected at the end of reperfusion. The renal function, histopathologic changes, and the expression levels of pro-inflammatory cytokines [interleukin-8(IL-8), tumor necrosis factor alpha(TNF-α) and IL-6] in serum and renal tissue homogenate were assessed. Moreover, the effects of Fenofibrate on activating phosphoinositide 3 kinase/protein kinase B(PI3K/Akt) signaling and peroxisome proliferator-activated receptor-α(PPAR-α) were also measured in renal IRI. The results showed that plasma levels of blood urea nitrogen and creatinine, histopathologic scores and the expression levels of TNF-α, IL-8 and IL-6 were significantly lower in FEN group than in IRI group. Moreover, Fenofibrate pretreatment could further induce PI3K/Akt signal pathway and PPAR-α activation following renal IRI. These findings indicated PPAR-α activation by Fenofibrate exerts protective effects on renal IRI in mice by suppressing inflammation via PI3K/Akt activation. Thus, Fenofibrate could be a novel therapeutic alternative in renal IRI. 展开更多
关键词 FENOFIBRATE renal ischemia/reperfusion injury activating phosphoinositide 3 kinase/protein kinase B INFLAMMATION
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Effect of Shenfu injection on ischemia-reperfusion injury of rat liver graft 被引量:3
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作者 Wei-Hua Zhu, Xi-Sheng Leng and Ji-Ye Zhu Department of Hepatobiliary Surgery, Peking University People’s Hospital, Beijing 100044, China 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2006年第2期205-209,共5页
BACKGROUND: It is reported that Shenfu injection (an injection prepared from traditional Chinese medicines red ginseng and aconite root) can decrease the extent of ischemia-reperfusion injury to many organs, such as t... BACKGROUND: It is reported that Shenfu injection (an injection prepared from traditional Chinese medicines red ginseng and aconite root) can decrease the extent of ischemia-reperfusion injury to many organs, such as the heart and kidney. We therefore investigated the effect of Shenfu injection on ischemia-reperfusion injury of rat liver graft and its mechanism. METHODS: Male Sprague Dawley (SD) rats were used as a model for isogeneic orthotopic liver transplantation. Sixty rats were randomly devided into two groups (30 in each group). The recipient was given intravenous Shenfu injection immediately before the removal of the liver in the Shenfu group and normal saline of the same volume in the control group. At 3, 6 and 24 hours after the reperfusion, blood and hepatic tissue were taken for examination. RESULTS: The levels of superoxide dismutase (SOD) and nitric oxide (NO) increased more significantly in the Shenfu group than in the control group (P <0.05). The levels of serum liver enzymes, hyaluronic acid (HA), malondialde-hyde (MDA), tumor necrosis factor-alpha(TNF-α), inter-leukin-1 (IL-1), endothelin -1 (ET-1) and liver cell apopto-sis index were lower in the Shenfu group than in the control group (P <0. 05). Microscopic examination revealed that the morphological changes of hepatic tissue were more severe in the control group than in the Shenfu group. CONCLUSIONS: Shenfu injection has protective effect on ischemia-reperfusion injury of rat liver graft. It inhibits the production of oxygen free radical and the activation of Kupffer cells, decreases apoptosis of liver cell, and improves microcirculation. 展开更多
关键词 liver transplantation reperfusion injury Shenfu injection
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Effects of Lipoteichoic Acid induced Delayed Preconditioning on Ischemia-reperfusion Injury in Isolated Rat Hearts 被引量:2
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作者 马世玉 向继洲 +1 位作者 吴基良 胡本容 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2003年第3期230-233,共4页
To explore the potential of lipoteichoic acid (LTA) induced cardioprotection against ischemia-reperfusion (I/R) injury in isolated rat hearts and whether endogenous nitric oxide (NO) participates in the protection, th... To explore the potential of lipoteichoic acid (LTA) induced cardioprotection against ischemia-reperfusion (I/R) injury in isolated rat hearts and whether endogenous nitric oxide (NO) participates in the protection, the rats were pretreated with LTA (1 mg/kg, i p ) 24 h before the experiment, and the isolated hearts were subjected to 30 min no-flow normothermic global ischemia and 60 min reperfusion after a 20-min stabilization period by the langendorff method Cardiac functions were evaluated at the end of stabilization, and at 30 min, 60 min of reperfusion The amounts of MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase(LDH) and total NO oxidation products in the coronary effluent were measured spectrophotometrically at the end of reperfusion It was revealed that pretreatment with LTA could significantly improve the recovery of cardiac function, reduce the release of CK-MB and LDH, and increase the concentrations of NO in coronary effluent The protective effects were abrogated by pretreatment of the rats with L-NAME It was concluded that LTA could induce the delayed cardioprotection against I/R injury, and endogenous NO may be involved in the mechanisms 展开更多
关键词 PRECONDITIONING lipoteichoic acid myocardial reperfusion injury nitric oxide
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Tacolimus Postconditioning Alleviates Apoptotic Cell Death in Rats after Spinal Cord Ischemia-reperfusion Injury via Up-regulating Protein-Serine-Threonine Kinases Phosphorylation 被引量:2
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作者 潘峰 程艳香 +7 位作者 祝成亮 陶凤华 李章华 陶海鹰 贺斌 余铃 戢鹏 唐欢 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2013年第6期852-856,共5页
The effects of tacrolimus postconditioning on protein-serine-threonine kinases (Akt) phos- phorylation and apoptotic cell death in rats after spinal cord ischemia-reperfusion injury were investi- gated. Ninety male ... The effects of tacrolimus postconditioning on protein-serine-threonine kinases (Akt) phos- phorylation and apoptotic cell death in rats after spinal cord ischemia-reperfusion injury were investi- gated. Ninety male SD rats were randomly divided into sham operation group, ischemia-reperfusion group and tacrolimus postconditioning group. The model of spinal cord ischemia was established by means of catheterization through femoral artery and balloon dilatation. The spinal cord was reperfused 20 min after ischemia via removing saline out of balloon. The corresponding spinal cord segments were excised and determined for Akt activity in spinal cord tissue by using Western blotting at 5, 15, and 60 min after reperfusion respectively. Spinal cord tissue sections were stained immunohistochemically for detection of the phosphorylated Akt expression at 15 min after reperfusion. Flow cytometry was applied to assess apoptosis of neural cells, and dry-wet weights method was employed to measure water content in spinal cord tissue at 24 h after reperfusion. The results showed that the activities of Akt in tarcolimus postconditioning group were significantly higher than those in ischemia-reperfusion group at 5, 15, and 60 min after reperfusion (P〈0.05, P〈0.01). The Akt activities reached the peak at 15 min after reperfu- sion in ischemia-reperfusion group and tacrolimus postconditioning group. The percentage of apoptotic cells and water content in spinal cord tissue were significantly reduced (P〈0.01) in tacrolimus postcon- ditioning group as compared with those in ischemia-reperfusion group at 24 h after reperfusion. It is concluded that tacrolimus postconditioning can increase Akt activity in spinal cord tissue of rats, inhibit apoptosis of neural cells as well as tissue edema, and thereby alleviate spinal cord ischemia-reperfusion injury. 展开更多
关键词 protein-serine-threonine kinases reperfusion injury spinal cord ischemia tacrolimus post- conditioning
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Protection of Veratrum nigrum L.var.ussuriense Nakai alkaloids against ischemia-reperfusion injury of the rat liver 被引量:5
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作者 Zhen-Zhen Wang Wei-Jie Zhao +7 位作者 Xue-Song Zhang Xiao-Feng Tian Yu-Zhu Wang Feng Zhang Jin-Chan Yuan Guo-Zhu Han Ke-Xin Liu Ji-Hong Yao 《World Journal of Gastroenterology》 SCIE CAS CSCD 2007年第4期564-571,共8页
AIM: TO investigate the protective effects and possible mechanisms of Veratrum nigrum L. var. ussuriense Nakai alkaloids (VnA) on hepatic ischemia/reperfusion (I/R) injury in rats. METHODS: Forty male Wistar rat... AIM: TO investigate the protective effects and possible mechanisms of Veratrum nigrum L. var. ussuriense Nakai alkaloids (VnA) on hepatic ischemia/reperfusion (I/R) injury in rats. METHODS: Forty male Wistar rats were randomly divided into four experimental groups (n = 10 in each): (A) Control group (the sham operation group); (8) I/R group (pretreated with normal saline); (C) Small-dose (10 μg/kg) VnA pretreatment group; (D) Large-dose (20 μg/kg) VnA pretreatment group. Hepatic ischemia/ reperfusion (Hepatic I/R) was induced by occlusion of the portal vein and the hepatic artery for 90 min, followed by reperfusion for 240 min. The pretreatment groups were administered with VnA intraperitoneally, 30 min before surgery, while the control group and I/R group were given equal volumes of normal saline. Superoxide dismutase (SOD) activity, myeloperoxidase (MPO) activity and nitric oxide (NO) content in the liver tissue at the end of reperfusion were determined and liver function was measured. The expression of intercellular adhesion molecule-1 (ICAM-1) and E-selectin (ES) were detected by immunohistochemical examinations and Western blot analyses. RESULTS: The results showed that hepatic I/R elicited a significant increase in the plasma levels of alanine aminotransferase (ALT: 74.53 ± 2.58 IU/L vs 1512.54 ± 200.76 IU/L, P 〈 0.01) and lactic dehydrogenase (LDH: 473.48 ± 52.17 IU/L vs 5821.53 ± 163.69 IU/L, P 〈 0.01), as well as the levels of MPO (1.97 ± 0.11 U/g vs 2.57 ± 0.13 U/g, P 〈 0.01) and NO (69.37 ± 1.52 μmol/g protein vs 78.39 ± 2.28 μmol/g protein, P 〈 0.01) in the liver tissue, all of which were reduced by pretreatment with VnA, respectively (ALT: 1512.54 ± 200.76 IU/L vs 977.93 ± 89.62 IU/L, 909.81 ± 132.76 IU/L, P 〈 0.01, P 〈 0.01; LDH: 5821.53 ± 163.69 IU/L vs 3015.44 ± 253.01 IU/L, 2448.75 ± 169.4 IU/L, P 〈 0.01, P 〈 0.01; MPO: 2.57 ± 0.13 U/g vs 2.13 ± 0.13 U/g, 2.07 ± 0.05 U/g, P 〈 0.01, P 〈 0.01; NO: 78.39 ± 2.28 μmol/g protein vs 71.11 ± 1.73 μmol/g protein, 68.58 ± 1.95 μmol/g protein, P 〈 0.05, P 〈 0.01). The activity of SOD (361.75 ± 16.22 U/rag protein vs 263.19 ± 12.10 U/rag protein, P 〈 0.01) in the liver tissue was decreased after I/R, which was enhanced by VnA pretreatment (263.19 ± 12.10 U/rag protein vs 299.40 ± 10.80 U/rag protein, 302.09 + 14.80 U/rag protein, P 〈 0.05, P 〈 0.05). Simultaneously, the histological evidence of liver hemorrhage, polymorphonuclear neutrophil infiltration and the overexpression of ICAM-1 and E-selectin in the liver tissue were observed, all of which were attenuated in the VnA pretreated groups. CONCLUSION: The results demonstrate that VnA pretreatment exerts significant protection against hepatic I/R injury in rats. The protective effects are possibly associated with enhancement of antioxidant capacity, reduction of inflammatory responses and suppressed expression of ICAM-1 and E-selectin. 展开更多
关键词 Veratrum nigrum L.var. ussuriense Nakaialkaloids Hepatic Ischemia/reperfusion injury Intracellular adhesion molecule-i E-SELECTIN
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