Silibinin improves nonalcoholic fatty liver by regulating the expression of miR-122: An in vitro and in vivo study

Silibinin is a flavonoid that improves fatty liver and insulin resistance. To elucidate the effect of silibinin on lipid deposition and the potential molecular mechanism, the present study conducted in vivo and in vitro experiments. In the in vivo experiments, mice were randomly divided into control, high-fat and silibinin groups, while HepG2 cells were randomly divided into control, palmitic acid intervention and silibinin intervention groups. The mRNA, protein and miR-122 expression associated with hepatic lipid metabolism were detected in each group. The results demonstrated that silibinin reduced the triglyceride content, miR-122 expression and the mRNA and protein expressions of fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC). Silibinin increased the mRNA and protein expression of carnitine palmitoyl transferase 1A (CPT1A). In the present study, HepG2 cells cultured with palmitate were treated with silibinin following overexpression of micro RNA (miR) 122. The results demonstrated that the mRNA and protein expression of FAS and ACC was increased, while that of CPT1A was decreased. Therefore, it could be deduced that silibinin improved lipid metabolism by reducing the expression of miR-122 and inhibiting the expression of miR-122 may be a new therapeutic target to improve fatty liver disease.

Automated summary

Silibinin improves fatty liver by reducing miR-122 expression and increasing CPT1A expression, ultimately leading to a decrease in hepatic lipid deposition. The modulation of miR-122 expression may serve as a novel therapeutic target for improving fatty liver disease.