MiR-141-3p Inhibits Oxidative Stress Damage in Diabetic Wounds by Regulating the KEAP1/Nrf2 Axis
Objective To explore the protective effect and molecular mechanism of miR-141-3p on keratinocytes under oxi-dative stress.Methods Keratinocytes were pretreated with hydrogen peroxide(H2O2)in vitro,and miR-141-3p mimics/inhibitor and siKEAP1 were employed to study the effect of miR-141-3p on the KEAP1/Nrf2 signaling pathway.Cell via-bility,mRNA expressions,protein expressions,miR-141-3p target genes,and intracellular ROS were detected using the CCK-8 assay,qRT-PCR,Western blot,dual-luciferase reporter assay system,and the DCFH-DA probe,respectively.Enzyme-linked immunosorbent assay,EDU method,and cell scratch assay were used to determine the antioxidant enzyme activity,cell proliferation function,and cell migration function,respectively.Results Overexpression of miR-141-3p en-hanced the proliferation and migration of keratinocytes under H2O2,reduced intracellular ROS,and increased SOD and GSH-px activities.MiR-141 could target and negatively regulate KEAP1,and up-regulate the expressions of Nrf2 and HO-1 to suppress oxidative stress.SiKEAP1 inhibited the pro-proliferation,pro-migration,and anti-oxidative effects of miR-141-3p.Conclusion miR-141 effectively reduces H2O2-induced oxidative stress damage in keratinocytes through the KEAP1/Nrf2 signaling pathway and promote their proliferation and migration,thereby facilitating diabetic wound healing.
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