CAJ | 학술논문

目的探讨Wnt7a-Akt/mTOR信号通路在肾衰营养胶囊改善慢性肾衰竭(CRF)大鼠骨骼肌萎缩中的作用及机制.方法采用切除5/6肾的方法制作CRF模型,予4%酪蛋白饲料喂养制作CRF营养不良大鼠模型.将大鼠随机分为正常组、模型组、中药组和开同组.采用组织病理学检测TA横截面积并计算肌纤维面积分布;采用同位素14+C-苯丙氨酸掺入法检测肌肉蛋白合成;采用Western blot检测Wnt7a-Akt/mTOR信号通路中的蛋白表达.结果肾衰营养胶囊增加了CRF大鼠体质量和骨骼肌质量的作用,形态学表现为TA横截面积增加,促进蛋白质合成增加以及骨骼肌组织Wnt7a-Akt/mTOR信号通路中蛋白表达上调.结论肾衰营养胶囊具有改善CRF模型大鼠骨骼肌萎缩的作用,其机制可能上调骨骼肌Wnt7a-Akt/mTOR信号通路和促进骨骼肌蛋白质合成相关.
목적 탐토Wnt7a-Akt/mTOR신호통로재신쇠영양효낭개선만성신쇠갈(CRF)대서골격기위축중적작용급궤제.방법채용절제5/6신적방법제작CRF모형,여4%락단백사료위양제작CRF영양불량대서모형.장대서수궤분위정상조、모형조、중약조화개동조.채용조직병이학검측TA횡절면적병계산기섬유면적분포;채용동위소14+C-분병안산참입법검측기육단백합성;채용Western blot검측Wnt7a-Akt/mTOR신호통로중적단백표체.결과 신쇠영양효낭증가료CRF대서체질량화골격기질량적작용,형태학표현위TA횡절면적증가,촉진단백질합성증가이급골격기조직Wnt7a-Akt/mTOR신호통로중단백표체상조.결론신쇠영양효낭구유개선CRF모형대서골격기위축적작용,기궤제가능상조골격기Wnt7a-Akt/mTOR신호통로화촉진골격기단백질합성상관.
Objective To observe the effect of Shenshuai Yingyang Capsule (SSYYJN) in ameliorating muscle atrophy in rats with chronic renal failure (CRF) and explore the role of Wnt7a-Akt/mTOR signal pathway in mediating this effect. Methods Male rats were randomly assigned to 5/6 nephrectomy group and sham-operated group, and the former group was further randomly divided into CRF model group, KA group, and SSYYJN group. The size of anterior tibia muscle was examined microscopically with HE staining. Protein synthesis in the soleus muscle was investigated by 14C-phenylalanine experiment, and the expression of Wnt7a, frizzled-7, phospho-Akt, phospho-mTOR and GAPDH were detected with Western blotting. Results The body weight, the wet and dry weight, cross-sectional area, and muscle protein synthesis of the anterior tibia muscles, and expressions of the proteins in the Wnt7a/Akt signaling pathway all increased significantly in SSYYJN and KA groups as compared with those in the model group. Conclusion SSYYJN can effectively improve muscle atrophy in the rat model of CRF possibly by reversing the reduction in the expressions of Wnt7a/Akt signaling pathway proteins in the skeletal muscles.