〔Abstract〕 Objective To explore the effect mechanism of miR-483-5 p onpalmitic acid-injured podocytes. Methods Podocytes were treated with different concentrationsof palmitic acid, miR-483-5 p inhibitor, miR-483-5 p mimic and KLF2 plasmid, respectively. The binding relationship between miR-483-5 p and KLF2 was analyzed by starbase and dual-luciferase reporter assay. The cell viability was indicated by CCK-8 assay, the levelsof miR-483-5 p and KLF2 were indicated by qRT-PCR, the cell apoptosis was indicated by flow cytometry assay, and the levels ofmalonaldehyde(MDA), superoxide dismutase(SOD)were indicated by colorimetry assay, the protein levels of C caspase3, Nephrin and Podocin wereindicated by Western blot. Results Palmitic acid inhibitedviability(P<0.05) and promoted miR-483-5 p expression(P<0.05) onpodocytesin a concentration-dependent manner; miR-483-5 p inhibitor could partially reverse the inhibitory effect of palmitic acid(0.5 mmol/L) on cell viability(P<0.05), and reverse the stimulative effect on apoptosis(P<0.05) and oxidative stress(P<0.05).The miR-483-5 p was directly targeted to KLF2, and miR-483-5 p mimic further enhanced the inhibitory effect of palmitic acid on cell viability(P<0.05), Nephrin and Podocin expression levels(P<0.05), and enhanced the stimulative effect on oxidative stress(P<0.05) and C caspase3 expression level(P<0.05), which was partially reversed by KLF2 overexpression. Conclusion miR-483-5 p can regulate palmitic acid-induced podocytes injury through regulating KLF2 expression, which is helpful for the research of prognosis in patients with diabetic nephropathy.