MiR-199b-5p inhibition improves inflammation and oxidative stress damage in OA-induced non-alcoholic fatty liver disease through targeting SIRT1.

OBJECTIVES

Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease. This research investigates the role of miR-199b-5p in NAFLD development.

METHOD: This study enrolled 110 non-NAFLD patients and 90 NAFLD patients and collected their clinical data and serum samples. The level of miR-199b-5p was measured via qRT-PCR. Through experiments such as ELISA, biochemical assays, and CCK-8, the effects of miR-199b-5p on OA-induced inflammation, lipid metabolism, viability, and oxidative stress in HepG2 cells were analyzed. Meanwhile, the targeting relationship between miR-199b-5p and SIRT1 was verified through dual-luciferase assay and Western blot analysis.

RESULTS

miR-199b-5p was highly expressed in the NAFLD group and was significantly correlated with BMI, WC, TG, LDL-C, and HDL-C (P < 0.0001). ROC analysis demonstrated its diagnostic potential for NAFLD (AUC = 0.875, P < 0.0001). The OA-induced HepG2 cell model revealed that the miR-199b-5p inhibitor alleviated OA-induced suppression of cell viability, suppressed inflammation, reduced lipid levels, and alleviated oxidative stress. Furthermore, SIRT1 levels in the NAFLD group were significantly decreased and showed a significant negative correlation with miR-199b-5p (P < 0.0001).

CONCLUSIONS

miR-199b-5p is significantly elevated in the serum of NAFLD patients and shows a positive correlation with multiple metabolic indicators. This suggests its potential as a diagnostic biomarker for NAFLD. Additionally, inhibition of miR-199b-5p protects against OA-induced hepatocyte injury, partially through targeting SIRT1, which regulates inflammatory response and oxidative stress.