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目的观察胰岛素联合硒对糖尿病心肌病大鼠p38丝裂原激活蛋白激酶/CREB结合蛋白(p38MAPK/CBP)通路的影响。方法 50只SD大鼠随机分为空白对照组、糖尿病心肌病组、糖尿病心肌病胰岛素治疗组、糖尿病心肌病硒治疗组、糖尿病心肌病胰岛素联合硒治疗组。流式细胞术检测细胞周期;末端脱氧核糖核苷酸转移酶介导的缺口末端标记(TUNEL)法观察心肌细胞凋亡;Western blot法检测细胞周期蛋白D1(cyclin D1)、cyclin E、Bax、Bcl-2、p38MAPK/磷酸化p38丝裂原激活蛋白激酶(p-p38MAPK)、CBP及Ku70的水平;免疫共沉淀法检测Ku70的乙酰化。结果胰岛素联合硒明显抑制心肌细胞凋亡,增加Bcl-2表达,降低Bax、cyclin D1、cyclin E、p38MAPK/p-p38MAPK、CBP、Ku70和乙酰化Ku70的表达水平。结论胰岛素联合硒通过抑制p38MAPK/CBP通路抑制心肌细胞凋亡。
Objective To investigate the effect of insulin and selenium on p38 mitogen-activated protein kinase / CREB binding protein (p38MAPK / CBP) pathway in diabetic cardiomyopathy rats. Methods Fifty SD rats were randomly divided into blank control group, diabetic cardiomyopathy group, diabetic cardiomyopathy insulin treatment group, diabetic cardiomyopathy selenium treatment group and diabetic cardiomyopathy insulin combined selenium group. Flow cytometry was used to detect cell cycle. Cardiomyocyte apoptosis was observed by terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL). The expressions of cyclin D1, cyclin E, Bax, Bcl-2, p38MAPK / phospho-p38 mitogen-activated protein kinase (p-p38MAPK), CBP and Ku70 were detected by ELISA. Ku70 acetylation was detected by co-immunoprecipitation. Results Insulin combined with selenium significantly inhibited cardiomyocyte apoptosis, increased Bcl-2 expression and decreased the expression of Bax, cyclin D1, cyclin E, p38MAPK / p-p38MAPK, CBP, Ku70 and acetylated Ku70. Conclusion Insulin combined with selenium can inhibit cardiomyocyte apoptosis through inhibition of p38MAPK / CBP pathway.