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目的观测川芎嗪对缺血再灌注心肌细胞凋亡的影响及可能机制。方法结扎冠状动脉左前降支45min,再灌注180min复制大鼠心肌缺血再灌注(IR)模型,川芎嗪保护组(IR+TMP)在结扎冠状动脉前30min腹腔注射川芎嗪(20mg/kg)。以TUNEL法检测细胞凋亡率,免疫组化法分析Fas/FasL、Caspase-8及Caspase-3蛋白表达,荧光分析法测定Caspase-3活性。结果缺血再灌注(IR)组心肌细胞凋亡指数(23.47±3.88)较对照组(0.41±0.03)有显著性升高(P<0.01),Fas/Fasl,Caspase-8和Caspase-3蛋白表达及Caspase-3活性也显著高于对照组。川芎嗪保护组(IR+TMP)心肌细胞凋亡指数(1.8±0.25)较IR组有显著性降低(P<0.05),Fas/FasL、Caspase-8、Caspase-3蛋白及Caspase-3活性也均显著性低于IR组。结论川芎嗪对缺血再灌注心肌细胞凋亡有较好的拮抗作用,其机制可能与降低Fas死亡受体通路的信号转导有关。
Objective To observe the effects of tetramethylpyrazine on myocardial cell apoptosis induced by ischemia-reperfusion and its possible mechanism. METHODS: The left anterior descending coronary artery was ligated for 45 min, and reperfusion was performed for 180 min. The rat model of myocardial ischemia-reperfusion (IR) was established. Ligustrazine protection group (IR+TMP) was intraperitoneally injected with tetramethylpyrazine (20 mg/kg) 30 min before coronary artery ligation. The apoptosis rate of cells was detected by TUNEL method. The expression of Fas/FasL, Caspase-8 and Caspase-3 protein was analyzed by immunohistochemistry. The activity of Caspase-3 was determined by fluorescence analysis. Results The apoptosis index of myocardial cells in ischemia-reperfusion (IR) group was significantly higher than that in control group (0.41±0.03) (P<0.01). Fas/Fasl, Caspase-8 and Caspase-3 protein The expression and Caspase-3 activity were also significantly higher than the control group. The apoptosis index (1.8±0.25) of cardiomyocytes in IR group was significantly lower than that in IR group (P<0.05), and the activity of Fas/FasL, Caspase-8, Caspase-3, and Caspase-3 were also decreased. All significant lower than the IR group. Conclusion Ligustrazine has a good antagonistic effect on myocardial cell apoptosis induced by ischemia-reperfusion, and its mechanism may be related to the decrease of signal transduction of Fas death receptor pathway.