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BACKGROUND We aimed to investigate the function and its possible mechanisms of long non-coding RNA (lncRNA) in acute myocardial infarction (AMI) model. METHODS Patients with AMI and normal volunteers were collected from our hospital. Sprague Dawley (SD) rats were induced into vivo model of AMI. H9c2 cells were treated with H2O2 to generate injury model. RESULTS A significantly lower serum gene expression of lncRNA CASC2 was detected.. In rat models of AMI, lncRNA CASC2 gene expressions in heart tissue of mice with AMI were decreased. In vitro model, down-regulation of lncRNA CASC2 increased reactive oxygen species (ROS) -induced oxidative stress; LncRNA CASC2 induced NADPH oxidase (NOX-2) expression and suppressed miR-18a expression; MiR-18a promoted reactive oxygen species (ROS)  -induced oxidative stress; Down-regulation of miR-18a decreased ROS-induced oxidative stress. The inhibition of miR-18a reversed the effects of CASC2 down-regulation on ROS-induced oxidative stress in vitro model of AMI. The activation of miR-18a reversed the effects of CASC2 on ROS-induced oxidative stress in vitro model of AMI. CONCLUSION These data for the first time suggest that lncRNA CASC2 have better protective effects on AMI which could be reduce oxidative stress through their carried miR-18a and subsequently down-regulating the SIRT2/ROS pathway. This article is protected by copyright. All rights reserved.