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Protective effects of betaine on ischemia-reperfusion injury through rOS pathway in rat

中国药理学与毒理学杂志 2017年第5期31卷 465-466页

作者： XUE Shuang JiA Xiao-ying ZHOU Lu GAO Shan institute of Pharmacology Taishan Medical University

Betaine have protective effects on liver,cardiovascular system,and cancer,but there is no report about i/r injury in heart. So the purpose of this experiment is to study the effect of betaine on i/r injury by Langendorff model and to discuss the mechanisms. SD rat were randomly divided into 4groups: control group(perfused with KH buffer),10^(-4)mol·L^(-1),5×10^(-4)mol·L^(-1),and 10^(-3)mol·L^(-1)(perfused with betaine in different concentration respectively for 10 min before ischemia followed by KH buffer perfused). During the experiment we detected LVEDP,LVDP,dp/dt,and store the tissue to do western blot and TTC staining. The result showed that in control group the recovery rate is 19.6%,after pretreatment of betaine the recovery rate all increased significantly and in a dose-dependent manner. The LVEDP is markedly decreased in betaine treatment groups compare to control group. Coronary flow only in highest betaine treatment group(10^(-3)mol·L^-) is markedly increased compare to control group,other two groups have no change. Western blotting showed that SOD level is significantly increased in betaine treatment group compare to control group and in a dose dependent manner. TTC staining suggested that infarction size is reduced in betaine treatment group compare to control group. Above all,the results suggest that betaine have protect effect on i/r injury in heart and this effect may relate to rOS signaling pathway.

关键词： betaine i/r injury SOD

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Cardioprotective effects of Guanxinshutong （GXST） against myocardial ischemia/ reperfusion injury in rats

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Journal of Geriatric Cardiology 2012年第2期9卷 130-136页

作者： Zhuo Llang Li-Feng Llu Tian-Ming Yao Yu Huo Ya-Ling Han Department of Cardiology Shenyang Northern Hospital Shenyang 110016Liaoning ProvinceChina Department of Cardiology Xijing HospitalThe Fourth Military Medical UniversityXi'an 710032Shaanxi ProvinceChina Department of lnstitute of Geriatric Cardiology Chinese PLA General Hospital 28 Fuxing Road100853 BeijingChina

Background The protective effects against reperfusion injury of cardioprotective drugs have recently been evaluated and found to be inadequate. Guanxinshutong （GXST）, a combination of the traditional herb and Mongolian medicine, is effective and safe in treating angina pectoris in clinical trials. We assess the cardioprotective effects of GXST against myocardial ischemia and reperfusion （Mi/r） injury in rats and explore its possible mechanism. Methods Forty-five male Sprague Dawley rats were randomized into three groups： non-Mlfr group （Sham, n = 15）, MUr group treated with vehicle （Control, n = 15） and Mi/r group treated with GXST （Drug, n = 15）. Mi/r was induced by ligation of the left anterior descending coronary artery （LAD） for 30 minutes, followed by 2/24 hour reperfusion in the Control and Drug groups. in the Sham group, the LAD was exposed without occlusion. GXST powder （in the Drug group） or saline （in the Control and Sham groups） were administered via direct gastric gavage from 7 day prior to surgery. Blood samples were collected from the carotid artery （10 rats each group） after 2 hours of reperfusion, to determine the levels of tumor necrosis factor-or （TNF-ct）, interleukin-1 ~ （iL-113）, interleukin-6 （iL-6） and intercellular adhesion molecule-1 （iCAM-1） using enzyme-linked immunosorbent assays. The animals were then sacrificed and the hearts were harvested for histopathology and western blot analysis. infarct size was measured in the remaining five rats in each group after 24 hours reperfusion. results GXST significantly decreased levels of TNF-ct, iL-1β, iL-6, iCAM-1, apoptosis index （Ai） and infarct size. GXST also obviously inhibited nuclear factor kappa B （NF.r,B） activity when compared with the Control group （all P 〈 0.05）. Conclusions GXST is effective in protecting the myocardium against Mi/r injury in rats. its possible cardioprotective mechanism involves inhibition of the inflammatory response and apoptosis following Mi/r injury.

关键词： i/r injury NF-r.B inflammation Apoptosis Chinese herbal Guanxinshutong

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Mediated protective effect of electroacupuncture pretreatment by mir-214 on myocardial ischemia/reperfusion injury

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Journal of Geriatric Cardiology 2014年第4期11卷 303-310页

作者： Pei-Yu LiU Yi TiAN Shi-Yuan XU Department of Anesthesiology ZhuJiang Hospital of Southern Medicine University Guangzhou 510282 Guangdong Province China Department of Anesthesiology Hainan Provincial Corps Hospital of Chinese People's Armed Police Forces Haikou 570203 Hainan Province China Department of Anesthesiology Haikou People's Hospital Haikou 570203 Hainan Province China

Background Electroacupuncture pretreatment plays a protective role in myocardial ischemia/reperfusion （i/r） injury and microrNAs （mirNAs） could act on various facets of cardiac function. However, the role of mirNAs in the cardioprotection by electroacupuncture pre-treatment on myocardial i/r injury remains unknown. The purpose of the study was to examine whether mir-214 was involved in cardio-protection by electroacupuncture. Methods Using rat myocardial i/r model, we examined the role of electroacupuncture pretreatment in myocardial i/r injury and analyzed the changes in the expression of mir-214. in addition, i/r was simulated in vitro by performing oxy-gen-glucose deprivation （OGD） on H9c2 cell cultures, and the effect of electroacupuncture pretreatment on i/r injury as well as expressional level of mir-214 were examined in vitro. Furthermore, the mir-214 mimic was transfected into OGD-treated H9c2 cells, we analyzed the cell apoptosis, lactate dehydrogenase （LDH） and creatine kinase （CK） activities, intracellular free Ca2＋concentration （[Ca2＋]i） as well as the relative protein levels of sodium/calcium exchanger 1（NCX1）, BCL2-like 11 （BiM）, calmodulin-dependent protein kinase iiδ（CaMKiiδ） and Cyclophilin D （CypD）. results The in vivo results revealed that compared with the i/r group, the electroacupuncture pretreatment group showed significant decreased myocardial infarct size, as well as the increased indices of the cardiac function, including heart rate, mean arterial pressure, left ventricular systolic pressure and maximal rate for left ventricular pressure rising and declining （±dp/dt max）. in addition, electroacupuncture pretreatment could inhibit the elevation of LDH and CK activities induced by i/r injury. The quantitative PCr （qPCr） results demonstrated electroacupuncture pretreatment could provide cardioprotection against myocardial i/r injury in rats with mir-214 up-regulation. in the meanwhile, in vitro, electroacupuncture pretreatment protected H9c2 c

关键词： i/r injury mir-214 Electroacupuncture Protective effect

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Dephosphorylation of cardiomyocyte Cx43 is associated with myocardial ischemia and reperfusion injury

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Journal of Nanjing Medical University 2009年第3期23卷 163-167页

作者： Zhijuan Cao Xuan Xu Linli Que Qi Chen Yuehua Li Department of Pathophysiology Nanjing Medical University Nanjing 210029 China

Objective：Myocardial ischemia/reperfusion（i/r） injury is the leading cause of death in the world. However, the details of the mechanism of its pathophysiology are still unknown. The present study was designed to investigate the role of connexin 43（Cx43） in acute models of myocardial i/r injury. Methods： Male C57BL/6 mice were subjected to myocardial ischemia（45 min） followed by reperfusion（4 hrs） in vivo. The whole operation was monitored using a two-lead ECG. Hearts were harvested and the level of protein was assessed by western blot analysis. Haematoxylin and Eosin（HE） staining was used to detect the extent of neutrophil infiltration. The expression level of iL-6 was detected by ELiSA. results： A murine myocardial i/r injury model was constructed successfully. Phosphorylated Cx43 decreased 83. 45% while non-phosphorylated Cx43 increased 1.62- fold in the myocardium after i/r injury. Neutrophil infiltration and the expression of the inflammatory cytokine iL-6 increased in the myocardium following i/r. Conclusion： During myocardial i/r injury, cardiomyocyte Cx43 is dephosphorylated, and this may be associated with an inflammatory response.

关键词： myocardium i/r injury connexin 43 inflammatory response

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Adiponectin confers neuroprotection against cerebral ischemia-reperfusion injury through activating the cAMP/PKA-CrEB-BDNF signaling

Adiponectin confers neuroprotection against cerebral ischemi...

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第十四届中国医师协会神经外科医师年会

作者： Hao Bai Lei Zhao Haixiao Liu Hao Guo Wei Guo Longlong Zheng Xunyuan Liu Xun Wu Jianing Luo Xia Li Li Gao Dayun Feng Yan Qu Department of Neurosurgery Tangdu HospitalFourth Military Medical University

ischemic stroke is a severe cerebrovascular disease. Although great progress has been made, the consequent ischemia-reperfusion（i/r） injury is inevitable and affects the therapeutic effect. Adiponectin（APN） is a fatderived plasma protein that has beneficial actions on cardiovascular disorders. The present study aims to investigate the effect of APN on i/r injury and the potential underlying mechanisms. in step 1, APN were administered for three times（once every 8 h） 24 h before middle cerebral artery occlusion（MCAO）. The results indicated that APN treatment reduced infarct volume, neurological deficits and brain water content after i/r injury. Meanwhile, APN was proved to increase the expression of cAMP, PKA, CrEB, and BDNF. in step 2, mice were randomly assigned into the Vehicle + i/r, APN + i/r, PKA activator + i/r, PKA inhibitor + APN + i/r groups. PKA activator, PKA inhibitor, as well as APN were administered for three times before MCAO. The results indicated that PKA inhibitor downregulated the expressions of cAMP, PKA, CrEB, and BDNF which subsequently weakened the protective effects of APN on cerebral i/r injury. in conclusion, our findings further suggest that APN exerts protective effect against cerebral i/r injury might through the cAMP/PKA-CrEB-BDNF signaling pathway. APN is a novel candidate in the treatment of i/r diseases in the future.

关键词： Adiponectin Stroke i/r injury PKA BDNF

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