首页> 美国卫生研究院文献>World Journal of Gastroenterology >Ursodeoxycholic acid ameliorates hepatic lipid metabolism in LO2 cells by regulating the AKT/mTOR/SREBP-1 signaling pathway
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Ursodeoxycholic acid ameliorates hepatic lipid metabolism in LO2 cells by regulating the AKT/mTOR/SREBP-1 signaling pathway

机译:熊去氧胆酸通过调节AKT / mTOR / SREBP-1信号通路改善LO2细胞的肝脂质代谢

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摘要

BACKGROUNDNonalcoholic fatty liver disease (NAFLD), the most common chronic liver disease, can progress into nonalcoholic steatohepatitis (NASH), cirrhosis, and even hepatocellular carcinoma. Bile acids such as ursodeoxycholic acid (UDCA) play an essential role in the pathogenesis of NAFLD by regulating the level of sterol regulatory element-binding protein (SREBP) 1c, but the underlying regulatory mechanism remains elusive. Increased evidence indicates that the AKT/mTOR/SREBP-1 signaling pathway is a key pathway to regulate hepatic cellular lipid metabolism. UDCA may regulate the AKT/mTOR/SREBP-1 signaling pathway to ameliorate hepatic lipid metabolism.
机译:背景技术非酒精性脂肪性肝病(NAFLD)是最常见的慢性肝脏疾病,可以发展为非酒精性脂肪性肝炎(NASH),肝硬化,甚至是肝细胞癌。胆汁酸,例如熊去氧胆酸(UDCA)通过调节固醇调节元件结合蛋白(SREBP)1c的水平在NAFLD的发病机理中起着至关重要的作用,但其潜在的调节机制仍然难以捉摸。越来越多的证据表明,AKT / mTOR / SREBP-1信号传导途径是调节肝细胞脂质代谢的关键途径。 UDCA可能调节AKT / mTOR / SREBP-1信号通路来改善肝脂质代谢。

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