miR-29b-3p靶向IGF1调控非酒精性脂肪肝脂质代谢及肝纤维化

目的 探讨miR-29b-3p在非酒精性脂肪肝疾病(NAFLD)模型中的表达情况,并确定miR-29b-3p在脂质沉积和肝细胞纤维化中的潜在功能.方法 使用棕榈酸(PA)构建L02细胞NAFLD模型.通过RT-qPCR或Western blot测定细胞中miR-29b-3p和胰岛素样生长因子-1(IGF-1)的表达水平...

miR-29b-3p regulates lipid metabolism and fibrosis by targeting IGF-1 in non-alcoholic fatty liver disease

Objective Circulating miR-29b has been reported to be positively correlated with nonalcoholic fatty liver disease(NAFLD).However,the role of miR-29b-3pI in NAFLD progression is unclear.The purpose of this study was to evaluate the expression of miR-29b-3p in NAFLD models and to identify the potential functions of miR-29b-3p in lipid accumulation and fibrosis in hepatocytes.Methods Palmitic acid(PA)-treated L02 cells were used as an in vitro cellular model of NAFLD.miR-29 b-3 p and insulin-like growth factor-1(IGF-1)expression levels were determined by RT-qPCR or Western blot.miR-29b-3p mimic/inhibitor or IGF-1 siRNA were transfected into L02 cells exposed to PA.Lipid accumulation was determined by oil red O staining,and triglyceride and total cholesterol assays.Direct interaction between miR-29b-3p and IGF-1 was determined by dual-luciferase reporter assay.Results The result revealed that miR-29b-3p was upregulated in our in vitro cellular model of NAFLD while IGF-1 concentrations decreased.miR-29b-3p inhibition significantly suppressed lipid accumulation and fibrosis in PA-treated L02 cells.miR-29b-3p targets IGF-1 and suppresses its expression in vitro.Interestingly,the effects of miR-29b-3p overexpression on lipid accumulation and fibrosis in PAtreated L02 cells was enhanced by IGF-1 silencing.Conclusions Our result suggested that miR-29b-3p has a negative regulatory effect on lipid accumulation and fibrosis in hepatocytes by targeting IGF-1.This study provides evidence that miR-29b-3p might be a promising therapeutic target for NAFLD.