Objective: To investigate the effect of miR-29b-3p targeting FoxO3 on non-alcoholic fatty liver disease (NAFLD). Methods: Human hepatocytes HL-7702 (L02) were transfected with miR-29b-3p inhibitor

NC inhibitor or pcDNAFoxO3. After palmitic acid (PA) treatment

oil red O staining was used to determine lipid accumulation

fully automatic biochemical analyzer to detect the content of triglycerides (TG) and total cholesterol (TC)

ELISA to detect the content of superoxide dismutase (SOD)

glutathione peroxidase (GSH-Px) and malondialdehyde (MDA)

RT-qPCR to detect the expression of forkhead box class O3 (FoxO3)

miR-29b-3p mRNA

Western blot to detect the expression of FoxO3 protein

and dual luciferase experiments to verify miR-29b-3p targeting FoxO3. Results: Compared with the control group

the expression of TG (2.05 ± 0.22) mmol/L

TC (7.80 ± 1.23) mmol/L

TNF-α (149.67 ± 8.96) %

IL-6 (157.00 ± 18.33) %

IL-8 (177.33 ± 24.58) %

miR-29b-3p (161.00 ± 13.0) %

MDA (0.456 ± 0.028) nmol/mL and the number of lipid droplets dyed red by Oil Red O in the PA group was significantly increased; the content of SOD (12.91 ± 0.53) ng/mL

GSH-Px (0.515 ± 0.038) ng/mL and the expression of FoxO3 (65.93 ± 4.56) % were significantly reduced; miR-29b-3p targeted FoxO3. Compared with PA group

PA + miR-29b-3p inhibitor group

PA + miR-29b-3p inhibitor + pcDNA-FoxO3 group significantly reduced the content of TG

TC

TNF-α

IL-6

IL-8

miR-29b-3p

MDA and the number of oil droplets dyed red by Oil Red O

and significantly increased the content of SOD and GSH-Px. Conclusion: MiR-29b-3p targeting FoxO3 can reduce PA-induced lipid accumulation and inflammation in L02 cells.