Protective mechanism of lncRNA KCNQ1OT1 targeting miR-132-5p against cell damage in Parkinson's disease
Objective To explore the protective mechanism of long non-coding RNA KCNQ1OT1(lncRNA KCNQ1OT1)targeting microRNA-132-5p(miR-132-5p)against cell damage in Parkinson's disease.Methods SH-SY5Y cells were induced with 1-methyl-4-phenylpyridinium ion(MPP+)to establish a cell model of Parkinson's disease or blank control.The expression of lncRNA KCNQ1OT1,miR-132-5p,reactive oxygen species(ROS),superoxide dismutase(SOD),malondialdehyde(MDA),interleukin-1β(IL-1β),interleukin-6(IL-6)tumor necrosis factor-α(TNF-α),apoptosis rate,and the expression of B-cell lymphoma2(BCL-2)and Bax proteins in SH-SY5Y cells were detected,aiming to verify the regulatory relationship between lncRNA KCNQ1OT1 and miR-132-5p.Results Compared with control(Con)group,the expression levels of lncRNA KCNQ1OT1 and miR-132-5p in MMP+ group were significantly higher(P<0.05).Both low expression of lncRNA KCNQ1OT1 and interference with expression of miR-132-5p could alleviate MMP+-induced oxidative stress and inflammatory damage of SH-SY5Y cells,inhibit cell death,and positively regulate expression of miR-132-5p by targeting lncRNA KCNQ1OT1.Over-expression of miR-132-5p reversed the oxidative stress,inflammatory damage and apoptosis of MMP+-induced SK-N-SH cells by low expression of lncRNA KCNQ1OT1.Conclusion LncRNA KCNQ1OT1 alleviated the oxidative stress,inflammatory damage,and apoptosis of MMP+-induced SK-N-SH cells by targeted inhibition of miR-132-5p expression.
long non-coding RNA KCNQ1OT1(lncRNA KCNQ1OT1)microRNA-132-5p(miR-132-5p)Parkinson's diseasecell injury
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