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p55TNFR选择性淋巴毒素对大鼠缺血再灌注后心脏损伤的保护作用 被引量:3

Protection against myocardial ischemia-reperfusion injury in rats by a novel selective lymphotoxin binding p55TNFR
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摘要 目的 研究p55TNFR选择性淋巴毒素对缺血-再灌注后心脏损伤的保护作用,并探讨其作用机制.方法 SD大鼠40只随机(随机数字法)分为4组,A组为假手术组,B组为大鼠心脏缺血-再灌注(I/R)模型组,C组为25 μg/(kg·d)野生型淋巴毒素(rhLTα)治疗组,D组为25 μg/ (kg·d)p55TNFR选择性淋巴毒素(rhLTα-Q107E)治疗组.各组在制备I/R模型后微量泵持续24h静脉滴注生理盐水或治疗药物,24h后检测血浆中心肌酶谱(AST、LDH、CK)、氧化/抗氧化指标(SOD、MDA、GSH-Px),硝基蓝四唑染色计算心肌梗死面积.结果 大鼠心脏缺血-再灌注(I/R)模型心肌梗死面积显著增高,心肌酶谱指标、MDA较假手术组明显升高(P<0.05),SOD和GSH-Px则明显降低(P<0.05).rhLTα-Q107E治疗组可逆转心肌缺血-再灌注后心肌酶谱指标、MDA的升高及SOD和GSH-Px的下降(P<0.05),而野生型rhLTα治疗组的作用不明显(P>0.05).结论 p5STNFR选择性淋巴毒素对大鼠心脏缺血-再灌注后的急性心脏损伤具有保护作用,其机制可能通过直接清除氧自由基、增加内源性抗氧化酶系统的活力而发挥保护作用. Objective To investigate the effect of a novel lymphotoxin with selectively binding to p55 tumor necrosis factor receptor (p55TNFR) on myocardial ischemia-reperfusion injury in rats in order to explore the mechanism.Methods A total of 40 SD rats were randomly (random number) assigned into four groups (n =10 in each),namely sham operation group (group A),I/R group (group B),wild type rhLTα treatment group (group C),and p55TNFR selective rhLTα (rhLTα-Q107E) treatment group (group D).After I/R model rats were established,various therapeutic agents or saline were given by continuous intravenous infusion for 24 h via a micropump.After 24 hours of treatment,serum myocardial zymogram,such as aspartate aminotransferase (AST),lactate dehydrogenase (LDH) and creatine kinase (CK),as well as superoxide dismutase (SOD),malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) activities were determined.Myocardial infarction size (MIS) was measured by nitro blue tetrazolium chloride (NBT) staining.Results Compared to sham operation group,MIS,AST,LDH,CK,MDA were increased,while the activities of SOD and GSH-Px were decreased.However,all the effects were significantly reversed by treatment with rhLTα-Q107E (P 〈 0.05) but not rhLTα (P 〉 0.05).Conclusions The rhLTα-Q107E plays a role in the protection against myocardial ischemia-reperfusion injury in rats by the mechanism of scavenging oxygen free radicals and increasing the activity of endogenous antioxidant system.
出处 《中华急诊医学杂志》 CAS CSCD 北大核心 2015年第10期1131-1134,共4页 Chinese Journal of Emergency Medicine
基金 上海市卫生计生系统重点专科建设项目(ZK2012A35)
关键词 p55TNFR 缺血-再灌注 心脏损伤 氧化应激 The rhLTα-Q107E plays a role in the protection against myocardial ischemia - reperfusion
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