黄芪对大鼠心肌缺血再灌注损伤细胞凋亡的影响

Protective Effects of Huangqi Against Ischemia/Reperfusion Injury in Rats

目的探讨黄芪对大鼠心肌缺血再灌注损伤时细胞凋亡的影响及可能的机制。方法雄性SD大鼠36只随机分3组:假手术组、模型组、黄芪治疗组,每组12只。采用结扎大鼠左冠状动脉前降支法制备心肌缺血再灌注模型。测定再灌注前静脉注入黄芪对损伤大鼠心肌组织中MDA,SOD生成的影响;免疫组化法检测大鼠心肌细胞bcl-2、Bax基因表达;电镜下观察其形态学改变。观察损伤大鼠心肌细胞凋亡的形成和黄芪的干预作用。结果 (1)黄芪组能减少心肌组织中MDA生成,并明显提高缺血再灌注组织中SOD的活力;(2)黄芪组中bcl-2表达明显增多,平均灰度值明显下降,与对照组比较有显著差异(P<0.01),Bax表达下降,但无统计学意义(P>0.05);(3)透射电镜观察显示假手术组未见凋亡的细胞;模型组和黄芪组均有凋亡的细胞存在,但黄芪组中凋亡细胞数较对照组明显减少。结论黄芪可能通过拮抗氧自由基、上调凋亡抑制基因bcl-2等作用,对心肌缺血再灌注损伤时时细胞凋亡有一定的防治作用。

Objective To investigate the effects and mechanism of huangqi on cardiomyocyte apoptosis after ischemia reperfusion.Methods 36 male Sprague-Dauley rats were randomly divided into three groups ： sham operating group,ischemia reperfusion group and treatment group,with each group of 12 rats.The left anterior descended（LAD） coronary artery was ligated to establish the ischemia/reperfusion heart model.The rats were injected huangqi before reperfusion.The concentrations of SOD,MDA in myocardial were measured.The expression of Bax and Bcl-2 genes were investigated by immunohistochemistry,the microstructure was observed by transmission electron mi-croscopy.Results（1）Huangqi decreased the MDA contents,the SOD activities improved.（2） Huangqi donot inhibit the expression of bax genebut significantly increased expression of Bcl-2 gene.（3） The Apoptosis was found in the ischemia/reperfusion group and huangqi group but were not observed in the sham-operation group by transmission electron microscopy.Conclusions The results indicate that huangqi can inhibit apoptosis induced by ischemia-reperfasion injury through resisting the damaging of free adical and increasing the expression of Bcl-2 gene.