〔Abstract〕 Objective To investigate the expression and mechanism of long non-coding RNA(lncRNA) metastasis-associated lung adenocarcinoma transcript 1(MALAT1) and microRNA-181 a(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 hydrogen peroxide(H2O2) treatment in AC 16 human myocardial cell line.siRNA targeting MALAT1(si-MALAT) and negative control siRNA(si-NC) were transfected into AC 16 cells,and the cells were divided into H202 treatment(H2O2) group,H2O2+si-NC group,and H2O2+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 Compared to the Normal group,the expression of MALAT1 was upregulated and the expression of miR-181a was downregulated in the AMI group(P<0.05),and there was a negative correlation between MALAT1 and miR-181a expression.The lncBase online prediction database and dual-luciferase reporter assay results had proven that MALAT1 could target and regulate the expression of miR-181a.Compared to the H2O2group,the H2O2+si-MALAT group showed increased cell viability(P<0.05),decreased TUNEL-positive rate(P<0.05),decreased expression levels of cleaved caspase-3 and Bax(P<0.05),and increased expression level of Bcl-2(P<0.05),while the H202+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 inhibition of miR-181a.