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作 者:凌叶盛 余舒杰[1] 周彬[1] 钱孝贤[1] LING Yesheng;YU Shujie;ZHOU Bin;QIAN Xiaoxiao(Third Affiliated Hospital of SunYat -san University,Guanghzou,Guangdong 510630)
出 处:《中国中医药科技》2018年第6期812-814,共3页Chinese Journal of Traditional Medical Science and Technology
基 金:国家自然科学基金项目(81370447);广东省自然科学基金博士启动项目(2016A030310203)
摘 要:目的:探讨红景天(Rhodiola rosea L.)多糖(CRP)的降血糖作用机制。方法:以链脲佐菌素结合高脂饲料喂养建立小鼠糖尿病模型,将CRP口服灌胃给药,连续28 d,进行小鼠肝糖原含量测定,Western Blot检测各组小鼠肝脏AKT、Phospho-Akt-Ser^(473)、PI3 Kinase p85、GSK-3β以及Phospho-GSK-3β-Ser^9蛋白的表达水平。结果:CRP能够增加小鼠肝糖原含量并且提高肝脏PI3K、p-AKT Ser^(473)及p-GSK-3βSer^9的表达量。结论:CRP通过调控肝脏PI3K/AKT/GSK3β信号通路,增加肝糖原合成,改善糖尿病小鼠肝糖原代谢。Objective:To investigate the hypoglycemic mechanism of Crude Rhodiola rosea L.polysaccha- rides (CRP)in diabetic mice.Method:STZ and high-fat diet induced diabetic model of mice were continu- ously ig administered with CRP for 28days.The hepatic glycogen content of each group mice was measured,the protein expression levels of PI3K,p -AKT Ser^473 and p -GSK -3β Set^9 were measured in the end of the ex- periments by Western Blot method.Results:CRP could increase the hepatic glycogen content of diabetic mice , raise PI3K ,phosphorylation of AKT (Ser473)and GSK-313(Ser9)expressions in mice liver.Conclusion: CRP can improve hepatic glycogen metabolism in STZ and high -fat diet induced diabetic mice.The activation of PI3K/Akt/GSK3β insulin signalling pathway involved in hepatic glycogenesis were considered the therapeutic mechanisms of CRP.
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