黄芪预处理对大鼠心肌缺血再灌注损伤的保护作用及其机制

目的 探讨黄芪对大鼠缺血再灌注心肌的保护作用及其机制.方法 采用结扎左冠状动脉的方法制备心肌缺血再灌注损伤动物模型.SD大鼠30只随机分为3组:对照组、缺血再灌注组(I/R)和黄芪预处理组(H+I/R).光镜和透射电镜下观察心肌病理变化,检测血清肌酸激酶(CK)、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量,以及心肌组织Na~+K~+-ATP酶(Na~+K~+-ATPase)、Ca~(2+)-ATP酶(Ca~(2+)-ATPase)活性.结果 ①黄芪预处理组光镜和透射电镜下心肌细胞变性坏死程度及心肌细胞超微结构形态改变较缺血再灌注组显著减轻;②黄芪预处理组大鼠血清中CK、LDH活性和MDA含量显著降低(P<0.05),SOD、Na+ K+-ATPase、Ca~(2+)-ATPase活性显著提高(P<0.05).结论 黄芪对大鼠冠状动脉结扎后再灌注心肌损伤具有明显的保护作用,其机制可能与改善心肌缺血再灌注冠状微循环与抗氧自由基生成、减轻钙超载等多种机制有关.

Protective effects of Huangqi against ischemia /reperfusion injury in rats

Objective To study the effects and mechanism of Huangqi against myocardium injury induced by ischemia and reperfusion in rats. Methods Totally 30 male Sprague-Dauley rats were randomly divided into three groups: control group (C group), ischemia/reperfusion group (I/R group), ischemic pretreatment with Huangqi group (H+I/R group), with 10 rats in each. The left anterior descending (LAD) coronary artery was ligated to establish the ischemia/reperfusion heart model. Huangqi was administered before the model was established in the H+I/R group. The pathologic changes of myocardial tissues (under light and electron microscopy), content of creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in serum, as well as activities of Na~+K~+-ATPase and Ca~(2+)-ATPase in myocardial tissues were observed. Results Light and electron microscopic examination showed that the necrotic degeneration and pathologic changes of myocardiocytes in Huangqi group were significantly milder than those in the model group. The levels of CK, LDH, MDA were decreased significantly in Huangqi group (P<0.05), the activities of SOD, Na~+K~+-ATPase and Ca~(2+)-ATPase in myocardial tissues in Huangqi group significantly increased (P<0.05). Conclusion Huangqi shows a significantly protective effect on myocardial I/R injury in rats. The mechanism may be related to multiple factors, including improving microcirculation, forming anti-oxygen free radicals and decreasing calcium overload.