热休克蛋白70与肝脏缺血预处理延迟保护效应_医学论文.docVIP

热休克蛋白70与肝脏缺血预处理延迟保护效应_医学论文 热休克蛋白70与肝脏缺血预处理延迟保护效应_医学论文 作者：王占明　鲁建国　赖大年　包国强　马庆久　吴金生 【关键词】 缺血预处理 　　关键词: 缺血预处理热休克蛋白70缺血-再灌注损伤 　　摘 要:目的 研究缺血预处理对大鼠肝脏缺血再灌注损伤后延迟保护效应的机制. 方法 建立大鼠肝脏缺血再灌注模型并进行缺血预处理，实验分组如下:①假手术组（Sham-op-eration，S组）②缺血再灌注组（ischemic reperfusion，I/R组）③缺血预处理组（ischemic preconditioning，PC组）④预处理加左旋硝基精氨酸组（preconditioning+L-NNA，PC+L组），各组再灌注后检测血清谷丙转氨酶（alanine aminotrans-ferase，ALT）及丙二醛（malondialdehyde，MDA）含量、热休克蛋白70（HSP70）免疫组化染色，肝组织石蜡切片HE染色及电镜观察. 结果 PC组ALT及MDA含量明显低于I/R组（0.01），肝组织损伤程度明显减轻PC+L组在0～3h阶段ALT和MDA含量与I/R组无显著区别（Pgt0.05），而在6～48h阶段则显著低于I/R组（0.01）但仍高于PC组（0.05）.HSP70免疫组化染色:PC组、PC+L组3～48h染色阳性率逐渐增多并显著高于I/R组（0.01）. 结论 NO和HSP70均对大鼠肝脏缺血再灌注损伤具有保护作用，HSP70可能是导致延迟保护效应的重要因素. 　　Keywords:ischemic preconditioningheat shock proteinsis-chemia-reperfusion injury 　　Abstract:AIM To assess the protection of HSP70’s and time course in the preconditioning（PC）in ischemia/reperfu-sion（I/R）injury in rat liver.METHODS 168SD rats were randomly divided into four groups:①S group:n=42，sham-operated control②I/R group:n=42，subjected to ischemia for70min③PC group:n=42，ischemia for5min and reperfusion for5min for twice，then subjected to is-chemia④PC+L group:n=42，the rats were administered L-NNA（10mg#12539kg-1 ）before preconditioning，and then were subjected to ischemia for70min.Serum level of alanine aminotransferase（ALT）and malondialdehyde（MDA）was detected during reperfution.Expression of HSP70in hepatic cell was analysed by histochemical technique.RESULTS Serum level of ALT and MDA of both I/R and PC+L group increased，compared with PC group（0.01）after reperfu-sion.There was not significant difference between I/R group and PC+L group during0～3h（Pgt0.05）but there was during6～48h（0.01）.The serum level of ALT and MDA was higher in PC+L vs PC group（0.05）but lower than I/R group during6～48h（0.01）.Expression level of HSP70in PC and PC+L group became gradually higher than I/R group during6～48h（0.01）.CONCLUSION NO and HSP70might be involved in the protection against liver ischemia/reperfusion injury an