LncRNA ZFAS1 ameliorates injury led by non-alcoholic fatty liver disease via suppressing lipid peroxidation and inflammation

Abstract

BackgroundNonalcoholic fatty liver disease (NAFLD) is known to aggravate metabolic disturbance and increase the risk of complications. The purpose of the present study was to explore the mechanism underlying the clinical effects of ZFAS1 on NAFLD. MethodsExpression of the ZFAS1 RNA was quantified in patients with NAFLD through reverse transcription-quantitative polymerase chain reaction. The correlations were assessed using Pearson's correlation coefficient test. The receiver operating characteristic curve was used to evaluate the identification of ZFAS1. Commercial kits were purchased to detect the pertinent parameters to establish mice models. Luciferase report assay was used to identify and confirm the presence of ZFAS1 ceRNA. ResultsThe increase of ZFAS1 expression in patients with NAFLD was noted and the high expression level may be considered a risk factor for NAFLD. In mouse models fed with high-fat diet (HFD), the expression levels of ZFAS1 were increased; furthermore, sh-ZFAS1 reversed ZFAS1 overexpression. HFD administration resulted in liver injury, which was indicated by increased lipid deposition, aggressive oxidative stress, and imbalanced inflammatory reaction. However, sh-ZFAS1 attenuated the abovementioned adverse effects of HFD. MiR-144-5p was a ceRNA of ZFAS1; in addition, the expression of miR-144-5p was reduced in HFD-managed models and patients with NAFLD. ZFAS1 could successfully regulate the expression levels of miR-144-5p. In the present study, the negative relationship between ZFAS1 and miR-144-5p was documented. ConclusionExcessive expression of ZFAS1 and its diagnostic potential was noted in patients with NAFLD. It was evident that ZFAS1 may be responsible for exacerbating the worsening of liver function.