【摘要】 目的:探讨科索亚对心力衰竭大鼠骨骼肌细胞的凋亡及Bcl-2和Bax蛋白表达的影响。方法:将38只SD大鼠随机分为4组:正常对照组(A组,n=8),心力衰竭组(B组,n=10),心力衰竭科索亚治疗1组(C组,n=10),心力衰竭科索亚治疗2组(D组,n=10)。B、C、D组分别腹腔一次性注射野百合碱30mg/kg。2周后,C组和D组分别用科索亚10mg·kg-1·d-1和30mg·kg-1·d-1灌胃2周,A组和B组则以生理盐水灌胃2周。2周后处死动物,以腓肠肌质量和体质量比作为骨骼肌萎缩的指标。TUNEL法检测腓肠肌细胞凋亡。免疫组织化学和免疫印迹法检测腓肠肌Bcl2、Bax的表达,并计算Bax/Bcl2的比值。结果:与A组相比,B组腓肠肌凋亡指数升高(P<0.01),Bcl2表达减少(P<0.01),Bax表达升高(P<0.05),Bax/Bcl2比值>1。与B组相比,C组和D组腓肠肌细胞凋亡指数降低(P<0.01);且C组和D组Bcl2表达升高(P<0.01),Bax表达减少(P<0.05),Bax/Bcl2比值均<1。结论:细胞凋亡可能是心力衰竭时骨骼肌萎缩的原因之一;科索亚可能通过改变Bax/Bcl2比值减轻心力衰竭时骨骼肌的凋亡和萎缩。更多还原

【Abstract】 Aim: To explore the effects of cozaar on the cell apoptosis and expression of Bcl-2 and Bax in skeletal muscle from rats with heart failure. Methods: A total of 38 SD rats were divided into 4 groups: normal control group (group A, n=8), heart failure group (group B,n=10),cozaar treatment group Ⅰ(group C,n=10), and cozaar treatment group Ⅱ(group D, n=10). Groups B, C, and D were induced heart failure by injecting monocrotaline 30 mg /kg.After 2 weeks, group C and D were treated with 10 mg·kg -1·d -1 and 30 mg·kg -1·d -1 cozaar by gavage, respectively.Group A and B were given normal saline by gavage. After additional 2 weeks, all rats were killed.Gastrocnemius weight/body weight ratio was served as index of muscle atrophy. Apoptosis of gastrocnemius was detected using TUNEL staining.The expressions of Bcl-2 and Bax in gastrocnemius were quantified by immunhistochemistry and immunoblot.Results: Compared with group A,the apoptosic index of skeletal muscle in group B was higher(P<0.01),the expression of Bcl-2 decreased(P<0.01) and expression of Bax increased(P<0.05). The ratio of Bax/Bcl 2 was more than 1. Compared with group B,the apoptosic index of skeletal muscle in group C and D was lower(P<0.01), expression of Bcl-2 increased(P<0.01), expression of Bax decreased(P<0.05), and the ratio of Bax/Bcl-2 was less than 1.Conclusion: Apoptosis plays an important role in skeletal muscle atrophy in rats with heart failure.Cozaar may alleviate the apoptosis and atrophy in heart failure rats by regulating the ratio of Bax/Bcl-2.更多还原