穴位埋线对心肌缺血再灌注过程自噬相关蛋白表达的影响

Expression of autophagy associated protein during myocardial ischemia reperfusion upregulated by acupoint catgut implantation

目的:探讨埋线对缺血再灌注损伤ZDF大鼠心肌Beclin-1、Bcl-2及P62蛋白表达的影响。方法:将24只雄性ZDF大鼠随机分为4组(n=6):空白组、缺血再灌注组、针刺组和埋线组。采用推管法制备心肌缺血再灌注损伤模型。ELISA法测定各组大鼠血清超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)含量;蛋白质印迹法检测各组大鼠心肌组织Beclin-1、Bcl-2及P62的表达;电镜观察心肌组织超微结构。结果:与空白组比较,其余3组大鼠血清SOD、GSH-Px含量均明显下降(P<0.01),心肌组织Beclin-1、Bcl-2及P62表达显著增强(P<0.01);与缺血再灌注组比较,针刺组及埋线组血清SOD、GSH-Px含量明显上升(P<0.01),心肌Beclin-1、Bcl-2表达明显升高,P62蛋白的表达显著降低(均P<0.01);电镜观察结果显示,与缺血再灌注组比较,针刺组及埋线组ZDF大鼠心肌损伤相对较轻,自噬泡数量增多。结论:埋线可能通过上调心肌中Beclin-1、Bcl-2及下调P62的表达激活自噬,从而有效保护缺血再灌注损伤心肌。

Objective： To investigate the effect of acupoint catgut implantation on the expressions of pro- tein Beelin-1, Bcl-2 and P62 in myocardium of ZDF rats with ischemia-reperfusion injury. Methods： Twenty-four male ZDF rats were randomly divided into four groups （n = 6 ） ：blank group, ischemia-reperfusion group, acupuncture group and acupoint catgut implantation group. Myocardial ischemia-reperfusion injury model was prepared by push tube method. The levels of superoxide dismutase （SOD） , glutathione peroxidase （GSH-Px） were measured by ELISA method. The protein expressions of Beclin-1, Bcl-2 and P62 were detected by Western blotting. The ultrastructure of myocardium was observed by electron microscope. Results： Compared with the blank group, the levels of SOD and GSH-Px in the other three groups were significantly decreased（P 〈 0.01 ）, and the expression of Beclin-1, Bcl-2 and P62 were increased（P 〈0.01 ） .Compared with isehemia-reperfusion group , the levels of SOD , GSH-Px in the acupuncture group and the catgut implantation group increased（P 〈 0.01 ） , the expression of Beclin-1 and Bcl-2 increased and the P62 protein decreased（P 〈 0.01 ）. Compared with the ischemia-reperfusion group, ZDF rats in the acupuncture group and the catgut implantation group had lower myocardial injury and increased number of autophagic vacuoles. Conclusion： Catgut implantation may protect myocardium against ischemia-reperfusion injury by activation of autophagy in myocardium.