The Role And Mechanism Of MicroRNA-181a In Nonalcoholic Fatty Liver Disease

【Aim】 This study mainly analyzed the expression level of micro RNA-181a(mi R-181a)in nonalcoholic fatty liver disease(NAFLD).To explore its mechanism of action in the lipid metabolism of NAFLD to reveal that mi R-181 a plays an important role in the occurrence and development of NAFLD.【Methods】Real-time quantitative PCR(q RT-PCR)was used to detect mi R-181 a expression in NAFLD patients and healthy controls,and palmitic acid(PA)-induced NAFLD cell models of human hepatoma carcinoma cells Hep G2 cells,human hepatocytes L02 cells and C57BL/6 mouse primary hepatocytes.The mi R-181 a inhibitor or mimic was used to transfect Hep G2 cells,L02 cells exposed to or not to PA as well as primary hepatocytes in vitro to alter mi R-181 a expression levels.Oil red O staining and triglyceride assays were used to assess lipid accumulation in hepatocytes.The bioinformatics method was used to predict the target gene of mi R-181 a,the dual luciferase reporter gene assay and q RT-PCR and Western blotting were used to verify the direct interaction of the target gene.The expression of peroxisome proliferatoractivated receptor-α(PPARα)overexpression plasmid vector was transfected in vitro,and the protein expression level of downstream lipid metabolism-related genes of PPARα was detected by q RT-PCR and Western blotting.【Results】The expression of mi R-181 a was significantly elevated in the serum of patients with NAFLD.Triglyceride assay and oil red O staining showed that PAinduced lipid accumulation in Hep G2 cells,L02 cells and mouse primary hepatocytes was significantly increased,and the expression level of mi R-181 a was also increased.Inhibition of expression using the mi R-181 a inhibitor resulted in increased expression of the target gene PPARα and its downstream lipid metabolism genes,and lipid accumulation in hepatocytes induced by PA was also significantly attenuated.Upregulation of mi R-181 a expression using mi R-181 a mimic resulted in down-regulation of PPARα and decreased expression of downstream genes,and increased lipid accumulation in hepatocytes.At the same time,increasing PPARα expression levels can counteract lipid accumulation in hepatocytes caused by mi R-181 a mimic.【Conclusions】The expression of mi R-181 a is closely related to the disorder of lipid metabolism in NAFLD.mi R-181 a can provide a new therapeutic strategy for NAFLD by regulating its target gene PPARα to participate in the regulation of lipid metabolism in NAFLD.