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首页> 外文期刊>Journal of Molecular Endocrinology >Zanthoxylum alkylamides ameliorate protein metabolism disorder in STZ-induced diabetic rats
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Zanthoxylum alkylamides ameliorate protein metabolism disorder in STZ-induced diabetic rats

机译:花椒烷基酰胺改善了STZ诱导的糖尿病大鼠的蛋白质代谢异常

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This study aimed to evaluate the protein metabolism effect of Zanthoxylum alkylamides and to explore the potential mechanism in streptozotocin (STZ)-induced diabetic rats. Diabetic rats were orally treated with 2, 4 and 8?mg per?kg?bw of alkylamides daily for 28 days. Alkylamides decreased the relative weight of the liver and food intake, significantly increased the relative skeletal muscle weight and significantly decreased the blood urea nitrogen levels. Insulin, insulin-like growth factor 1, total protein (TP) and albumin (ALB), globular proteins and ALB proteins/globulin protein levels in serum significantly increased. TP, RNA content and RNA/DNA ratio significantly increased in the skeletal muscle of diabetic rats. Real-time quantitative polymerase chain reaction results indicated that alkylamides significantly increased the mRNA expression of insulin receptor (InR), IGF1 and insulin-like growth factor 1 receptor (IGF1R) in the liver and skeletal muscle. Moreover, the mRNA and protein expression levels of PI3K, PKB and mTOR significantly increased, whereas those of atrogin-1, muscle ring finger 1 and FOXO in the skeletal muscle significantly decreased. Alkylamides may advance protein synthesis by the PI3K/PKB/mTOR signalling pathway and attenuate the catabolism of protein through the ubiquitin–proteasome pathway. Therefore, it was possible that alkylamides ameliorate protein metabolism disorders in diabetic rats by activating the mTOR pathway.
机译:这项研究旨在评估花椒烷基酰胺的蛋白质代谢作用,并探讨链脲佐菌素(STZ)诱导的糖尿病大鼠的潜在机制。糖尿病大鼠每天口服每公斤千克体重2、4、8和8mg烷基酰胺治疗28天。烷基酰胺降低了肝脏的相对重量和食物摄入量,显着增加了相对骨骼肌的重量,并显着降低了血尿素氮水平。血清中的胰岛素,胰岛素样生长因子1,总蛋白(TP)和白蛋白(ALB),球状蛋白和ALB蛋白/球蛋白的水平显着增加。糖尿病大鼠骨骼肌中TP,RNA含量和RNA / DNA比值显着增加。实时定量聚合酶链反应结果表明,烷基酰胺显着增加了肝脏和骨骼肌中胰岛素受体(InR),IGF1和胰岛素样生长因子1受体(IGF1R)的mRNA表达。而且,骨骼肌中PI3K,PKB和mTOR的mRNA和蛋白质表达水平显着增加,而atrogin-1,肌肉无名指1和FOXO的mRNA和蛋白质表达水平显着降低。烷基酰胺可以通过PI3K / PKB / mTOR信号传导途径促进蛋白质合成,并通过泛素-蛋白酶体途径减弱蛋白质的分解代谢。因此,烷基酰胺可能通过激活mTOR途径改善糖尿病大鼠的蛋白质代谢异常。

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