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目的观察阿霉素所致心衰大鼠心肌ErbB4蛋白表达和细胞凋亡及NRG-1β的干预作用。方法用60只SD雄性大鼠随机分为4组:阿霉素心肌病8周组(ADR1,n=10),阿霉素2 mg/kg,尾静脉注射,每周1次,连续注射8周;阿霉素心肌病12周组(ADR2,n=20),阿霉素2 mg/kg,尾静脉注射,每周1次,连续注射8周,之后普通喂养到12周;阿霉素心肌病+NRG-1治疗组(NRG,n=20),在注射ADR后8周后即开始给予neuregulin-1β10μg/(kg.d)尾静脉注射,连续5 d,之后喂养到12周;正常对照组(CON,n=10)。免疫印迹法(Western blot)检测ErbB4受体蛋白的表达;HE染色病理观察评分;TUNEL法观察心肌细胞凋亡。结果心肌细胞凋亡指数:与模型组相比,NRG治疗组凋亡指数显著降低(P<0.05);ErbB4蛋白表达:模型组第8周时表达明显高于正常组,模型组12周时表达较正常组明显减少;与模型组比较,NRG干预组ErbB4蛋白表达明显上调(P<0.05)。结论ErbB4蛋白表达在扩张型心肌病大鼠心肌中表达早期增强,随着病程延长明显下降;NRG-1β能够抑制扩张型心肌病大鼠心肌细胞凋亡并增加其受体ErbB4的表达。
Objective To observe the expression of ErbB4 and the apoptosis of myocardial cells induced by doxorubicin in rats with heart failure and the effect of NRG-1β. Methods Sixty SD male rats were randomly divided into 4 groups: adriamycin cardiomyopathy 8 weeks (ADR1, n = 10), doxorubicin 2 mg / kg, tail vein injection, once a week, continuous injection of 8 Weeks; doxorubicin cardiomyopathy 12 weeks group (ADR2, n = 20), doxorubicin 2 mg / kg, intravenous injection once a week, continuous injection for 8 weeks, then normal feeding to 12 weeks; doxorubicin Cardiomyopathy + NRG-1 treatment group (NRG, n = 20). Neuregulin-1β 10μg / (kg · d) was injected into tail vein after 8 weeks of ADR injection for 5 consecutive days and then for 12 weeks. Normal Control group (CON, n = 10). The expression of ErbB4 receptor protein was detected by Western blot. The pathological score was observed by HE staining. Cardiomyocyte apoptosis was observed by TUNEL method. Results Apoptosis index of cardiomyocytes: Compared with the model group, the apoptosis index of NRG treatment group was significantly lower (P <0.05). The expression of ErbB4 protein in model group was significantly higher than that in normal group at the 8th week Compared with the model group, the expression of ErbB4 protein in NRG intervention group was significantly increased (P <0.05). Conclusion The expression of ErbB4 protein in myocardium of rats with dilated cardiomyopathy increased early and decreased with the prolongation of duration. NRG-1β could inhibit cardiomyocyte apoptosis and increase the expression of its receptor ErbB4 in dilated cardiomyopathy rats.