Objective To investigate the expression and mechanism of long non-coding RNA(lncRNA)metasta-sis-associated lung adenocarcinoma transcript 1(MALAT1)and microRNA-181a(miR-181a)in a myocardial cell oxidative stress model.Methods The expression of MALAT1 and miR-181a in peripheral blood of 30 patients with acute myocardial infarction(AMI group)and 30 healthy controls(Normal group)was detected by qRT-PCR.Pearson correlation analysis was performed to determine the correlation between MALAT1 and miR-181a in AMI.The binding sites between MALAT1 and miR-181a were predicted using the lncBase online prediction database and validated by dual-luciferase reporter assay.An oxidative stress model of myocardial cells was established by hydro-gen peroxide(H2 O2)treatment in AC16 human myocardial cell line.siRNA targeting MALAT1(si-MALAT)and negative control siRNA(si-NC)were transfected into AC16 cells,and the cells were divided into H2 O2 treatment(H2 O2)group,H2 O2+si-NC group,and H2 O2+si-MALAT group.Cell proliferation activity was detected by CCK-8 assay,cell apoptosis was assessed by TUNEL assay,and the expression levels of cleaved caspase-3,Bcl-2-associated X protein(Bax),and B-cell lymphoma-2(Bcl-2)were determined by Western blot.Results Com-pared to the Normal group,the expression of MALAT1 was upregulated and the expression of miR-181a was down-regulated in the AMI group(P<0.05),and there was a negative correlation between MALAT1 and miR-181a ex-pression.The lncBase online prediction database and dual-luciferase reporter assay results had proven that MAL-AT1 could target and regulate the expression of miR-181a.Compared to the H2 O2 group,the H2 O2+si-MALAT group showed increased cell viability(P<0.05),decreased TUNEL-positive rate(P<0.05),decreased expres-sion levels of cleaved caspase-3 and Bax(P<0.05),and increased expression level of Bcl-2(P<0.05),while the H2 O2+si-NC group showed no significant changes(P>0.05).Conclusion LncRNA MALAT1 expression is elevated in AMI patients,which could promote oxidative stress-induced myocardial cell damage through targeted in-hibition of miR-181a.
维普
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