黄芪预处理对缺血再灌注大鼠肾脏缝隙连接蛋白43表达的影响

Effect of Radix Astragali on connexin 43 expression in a rat model of renal ischemic reperfusion injury

目的:观察黄芪对缺血再灌注大鼠肾脏缝隙连接蛋白43(Cx43)表达的影响,探讨Cx43在抗缺血再灌注损伤中的作用及其意义。方法:30只SD大鼠平均分为假手术组、缺血再灌注(IR)组、黄芪干预组(RA组),于再灌注2 h后检测肾组织匀浆丙二醛(MDA)、超氧化物歧化酶(SOD)水平;同时进行肾组织切片,经HE染色后进行中性粒细胞(PMN)计数及Paller评分;Tunel法观察肾组织细胞凋亡情况,量化肾损伤程度;蛋白质印迹法测定肾组织内Cx43蛋白表达水平。结果:黄芪干预组MDA水平明显低于IR组,SOD水平明显高于IR组;黄芪干预组PMN计数、Paller评分及细胞凋亡指数明显低于IR组;IR组Cx43蛋白表达明显低于假手术组,黄芪组明显高于IR组。结论:黄芪能够提高Cx43蛋白的表达,减轻肾缺血再灌注损伤。

Objective： To observe the effect of Radix Astragali on connexin43（Cx43） expression after renal ischemic reperfusion（IR） in rats,and investigate the effect of Cx43 in the protective mechanism of Radix astragali on renal ischemic reperfusion injury.Methods： Thirty SD rats were divided into three groups randomly（n=10）： Sham operated group（Sham-group）,ischemic reperfusion group（IR-group）,Radix Astragali group（RA-group）.The rats underwent 60-minute renal ischemic and 2-hour reperfusion.The contents of MDA and SOD were examined.The pathological changes of kidney tissue were investigated by hematoxylin-eosin（HE） staining;the figures of PMN and Paller-grades were counted at the same time.The apoptotic index was measured by Tunel.The expression levels of Cx43 protein of kidney tissue were examined by Western blot analysis.Results： The level of MDA in RA-group was significantly lower,while the activities of SOD was dramatically higher than those in IR group.There were significant pathological changes in renal tissues after ischemic/reperfusion.The index of PMN and Paller-grades were very high in IR-group while it significantly decreased in RA-group.The Tunel analysis showed that the apoptotic index of tubular epithelial cells in RA-group was apparently lower than that of IR-group;protein expression of Cx43 in IR-group was significantly decreased as compared with that of Sham-group.The protein expression of Cx43 in RA-group was significantly increased as compared with that of IR-group.Conclusion： Radix astragali could protect renal tissue from ischemic reperfusion injury by up-regulation of the Cx43 expression.