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.
关键词
长链非编码RNA/KCNQ1OT1/微小RNA-132-5p/帕金森病/细胞损伤
Key words
long non-coding RNA KCNQ1OT1(lncRNA KCNQ1OT1)/microRNA-132-5p(miR-132-5p)/Parkinson's disease/cell injury
维普
万方数据