NONHSAT098487.2 protects cardiomyocytes from oxidative stress injury by regulating the Notch pathway

Acute myocardial infarction has increasingly become a global health problem and is a primary cause of cardiovascular disease-related death. Although long noncoding RNAs have been reported to play an important role in various cardiovascular diseases, their protective effects on car-diomyocytes against reactive oxygen species-induced oxidative injury have nonetheless been poorly studied. The present study aims to explore the effect of a novel long noncoding RNA, NONHSAT098487.2, on cardiomyocyte injury induced by H2O2. The expression of NON-HSAT098487.2 and pathway-related genes was evaluated by quantitative real-time polymerase chain reaction. Cell viability, release of lactate dehydrogenase, and apoptosis levels were detected by cell counting kit-8, lactate dehydrogenase release assay, and flow cytometry analysis, respectively. The protein levels were estimated by western blotting. The results showed that NONHSAT098487.2 was expressed at a high level in peripheral blood mononuclear cells from acute myocardial infarction patients, which showed a positive correlation with the HS-TnT and CK-MB levels of patients. Furthermore, it is also upregulated in human AC16 cardiomyocytes treated with H2O2 or exposed to hypoxia/reoxygenation conditions. Knockdown of NON-HSAT098487.2 restrained the Notch signalling pathway and aggravated H2O2-induced car-diomyocyte oxidative stress injury. In contrast, overexpression of NONHSAT098487.2 activated the Notch signalling pathway and suppressed H2O2-induced oxidative stress injury. However, the Notch inhibitor DAPT weakened the protective effects of NONHSAT098487.2. Therefore, the novel lncRNA NONHSAT098487.2 may play a role in protecting cardiomyocytes from oxidative stress injury by regulating the Notch pathway.