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目的研究在体老龄大鼠心肌缺血再灌注模型钙调神经磷酸酶(CaN)活性变化和环孢素A(CSA)的细胞保护作用。方法实验用Wistar老龄大鼠随机分为假手术组(sham组)、缺血再灌注组(I/R组)及CSA组,CSA组给予CSA 10 mg/(kg.d)腹腔注射,10 d后建立大鼠在体心肌I/R模型,I/R组及CSA组结扎左冠状动脉前降支30 min复灌3 h,Sham组仅穿线,不结扎。定磷法检测CaN活性,流式细胞术检测心肌细胞凋亡率。结果I/R后CaN的活性升高,心肌细胞凋亡率增加。CSA干预后心肌CaN的活性比I/R组明显下降(P<0.05),心肌细胞凋亡率也显著下降(P<0.05)。结论老龄大鼠心肌I/R损伤时,应用CSA能够通过抑制CaN信号转导途径,降低心肌细胞凋亡率,产生心肌细胞保护作用。
Objective To study the changes of calcineurin (CaN) activity and cytotoxicity of cyclosporin A (CSA) in the model of myocardial ischemia reperfusion in aged rats. Methods The aged Wistar rats were randomly divided into sham group, I / R group and CSA group. The CSA group was given intraperitoneal injection of 10 mg / (kg.d) of CSA for 10 days After establishment of rat myocardium I / R model, the anterior descending branch of left anterior descending coronary artery was ligated for 30 min in I / R group and CSA group for 3 h. Sham group was only threaded and non-ligated. Determination of CaN activity by fixed phosphorus method, flow cytometry myocardial cell apoptosis rate. Results The activity of CaN increased after I / R, and the rate of cardiomyocyte apoptosis increased. After CSA intervention, the activity of CaN in myocardium was significantly lower than that in I / R group (P <0.05), and the apoptosis rate of myocardial cells was also significantly decreased (P <0.05). Conclusions CSA can decrease cardiomyocyte apoptosis and inhibit cardiomyocyte Ca2 + signal transduction pathway in cardiomyocyte injury induced by I / R in aged rats.