MicroRNA-205 ameliorates lipid accumulation in non-alcoholic fatty liver disease through targeting NEU1.

Abstract

The aim of this study was to explore the role of miR-205 in non-alcoholic fatty liver disease (NAFLD) and explore the underlying mechanism. High-fat diet (HFD) mice were used as an in vitro model of NAFLD. HepG2 and primary hepatocytes (PH) cells were treated with oleic acid (OA) and considered as in vitro models of NAFLD. qRT-PCR (quantitative real time polymerase chain reaction) and Western blot were respectively employed to investigate mRNA expression and protein expression level. Further analysis was then applied to analyze the underlying mechanisms. Livers were histologically examined using hematoxylin and eosin (H&E) and Oil Red O staining. TargetScan analysis and Luciferase assay were used to identify the target of miR-205. MiR-205 was upregulated and NEU1 was downregulated in both HFD-fed mice and OA-treated HepG2 and PH cells. The overexpression of miR-205 caused the decreased weight of body and liver, downregulation of liver triglyceride, and resulted in the enhancement of glycerol concentration, and finally suppressed lipid accumulation. In addition, the TargetScan analysis and Luciferase assay identified neuraminidase 1 (NEU1) as a novel target of miR-205. In vivo study suggested that the knockdown of NEU1 ameliorated lipid accumulation. Finally, the in vitro investigation showed that the overexpression of miR-205 alleviated lipid accumulation in OA-induced HepG2 and PH cells by targeting NEU1. Results revealed that miR-205 facilitated lipid accumulation by inhibiting NEU1 in NAFLD, suggesting that miR-205 might be a potential target for the therapeutic strategy for NAFLD.