ArticleBMC gastroenterology2025
MiR-199b-5p inhibition improves inflammation and oxidative stress damage in OA-induced non-alcoholic fatty liver disease through targeting SIRT1.
Article in BMC gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesNon-alcoholic fatty liver disease (NAFLD) is a chronic liver disease. This research investigates the role of miR-199b-5p in NAFLD development.
methodThis 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.
resultsmiR-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).
conclusionsmiR-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.
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