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[目的]探讨丹参酮ⅡA对大鼠缺血再灌注心肌细胞凋亡的影响。[方法]选取50只Wistar大鼠,随机分为5组:假手术组、缺血再灌注组和丹参酮ⅡA高中低剂量组。采用结扎大鼠左冠状动脉前降支方法制备心肌缺血再灌注模型,在缺血前10min分别向5组大鼠注射生理盐水4ml、生理盐水4ml、丹参酮ⅡA(16mg/kg、8mg/kg、4mg/kg)加入生理盐水共4ml。观察大鼠缺血45min再灌注2h时心电图改变情况;采用免疫组化方法对心肌组织中Bcl-2和Bax蛋白的表达。[结果]①缺血再灌注组缺血再灌注T波变化幅度与假手术组相比明显升高(P﹤0.01);不同剂量组缺血再灌注T波变化幅度比缺血再灌注组有不同程度的降低(P﹤0.05)。②缺血再灌注组缺血再灌注2h心律失常发生率与假手术组相比明显升高(P﹤0.01);不同剂量组缺血再灌注2h时心律失常发生率比缺血再灌注组有不同程度的降低(P﹤0.05)。③缺血再灌注组Bcl-2OD值、Bcl-2/Bax与假手术组相比明显降低(P﹤0.01);不同剂量组Bcl-2OD值、Bcl-2/Bax比缺血再灌注组有不同程度的升高(P﹤0.05)。缺血再灌注组BsxOD值与假手术组相比明显升高(P﹤0.01);不同剂量组BsxOD值比缺血再灌注组有不同程度的降低(P﹤0.05)。[结论]丹参酮ⅡA对大鼠缺血再灌注心肌有显著保护作用,其保护机制可能与上调Bcl-2及下调Bax蛋白表达,从而抑制缺血再灌注心肌细胞凋亡有关系。
[Objective] To explore the effect of Tanshinone ⅡA on cardiomyocyte apoptosis induced by ischemia-reperfusion in rats. [Methods] Fifty Wistar rats were randomly divided into 5 groups: sham operation group, ischemia reperfusion group and tanshinone Ⅱ A high and low dose group. The models of myocardial ischemia-reperfusion were established by ligation of left anterior descending coronary artery in rats. Rats in 5 groups were injected with 4 ml saline, 4 ml normal saline and tanshinone IIA (16 mg / kg, 8 mg / kg, 4mg / kg) was added to a total of 4ml of normal saline. The changes of electrocardiogram (ECG) were observed at 45 min after reperfusion and 2 h after ischemia in rats. The expressions of Bcl-2 and Bax protein in myocardium were detected by immunohistochemistry. [Results] ① The amplitude of T wave in ischemia-reperfusion group was significantly higher than that in sham-operated group (P <0.01). The amplitude of T wave in ischemia-reperfusion group was significantly higher than that in ischemia-reperfusion group Varying degrees of reduction (P <0.05). ② The incidence of arrhythmia at 2h after ischemia-reperfusion was significantly higher than that in sham-operation group (P <0.01). The incidence of arrhythmia at 2h after reperfusion was significantly higher than that of ischemia-reperfusion group Varying degrees of reduction (P <0.05). (3) The Bcl-2OD and Bcl-2 / Bax levels in ischemia-reperfusion group were significantly lower than those in sham operation group (P <0.01); Bcl-2OD and Bcl- Varying degrees of increase (P <0.05). The BsxOD of ischemia-reperfusion group was significantly higher than that of sham operation group (P <0.01). The BsxOD of ischemia-reperfusion group was lower than that of ischemia-reperfusion group (P <0.05). [Conclusion] Tanshinone IIA can protect myocardium from ischemia-reperfusion injury in rats. Its protective mechanism may be related to the up-regulation of Bcl-2 and the down-regulation of Bax protein, thereby inhibiting the apoptosis of myocardial cells during ischemia-reperfusion.