金香丹对缺血再灌注损伤大鼠心肌细胞凋亡的影响及其机制研究

摘要

Objective:To investigate the protective effects and the mechanism of Jinxiangdan Tablet on the apoptosis in rats with myocardial ischemia-reperfusion injury.Methods:60 male SD rats were randomly divided into 3 groups,the sham operation group,the ischemia-reperfusion group and the Jinxiangdan Tablet group.Rat models with myocardial ischemia-reperfusion injury were established by ligate left coronary arter (LCA) for 30min and followed by release of it with ligation for 120 min.The contents of serum malondialdehyde (MDA),the activities of serum superoxide dismutase (SOD),creatine kinase (CK) and lactate dehydrogenase (LDH) were detected at the end of reperfusion.TUNEL was used to detect the myocardial apoptosis index.Results:Jinxiangdan Tablets preconditioning significantly reduced the contents of serum MDA,lowered the activities of serum CK and LDH,enhanced the activities of serum SOD and decreased themyocardial apoptosis index (P ＜ 0.05 or 0.01).Conclusion:Jinxiangdan Tablet has preventive effects on myocardial ischemia-reperfusion injury in rats.It can alleviate myocardial apoptosis induced by oxygen free radicals.%目的 探讨金香丹对心肌缺血再灌注损伤模型大鼠心肌细胞凋亡的影响及其作用机制.方法 雄性SD大鼠60只随机分成假手术组、模型组及金香丹组,每组20只.金香丹组大鼠每日予金香丹片溶于生理盐水中灌胃,假手术组和模型组每天予等量生理盐水灌胃,共7d.末次灌胃后12h采用结扎左冠状动脉前降支30 min、再灌注60 min的方法建立大鼠心肌缺血再灌注损伤模型,再灌注末测定血清丙二醛(MDA)含量、超氧化物歧化酶(SOD)、肌酸激酶(CK)及乳酸脱氢酶(LDH)的活性,原位末端标记(TUNEL)法检测心肌细胞凋亡.结果 金香丹预处理减少再灌注末血清MDA含量、CK和LDH活性(P＜0.05或0.01),提高血清SOD活性(P＜0.01),降低心肌细胞凋亡率(P＜0.01).结论 金香丹预处理减轻心肌缺血再灌注损伤模型大鼠的脂质过氧化损伤,从而减轻氧自由基诱导的心肌细胞凋亡.