Silencing of long non-coding RNA HRIM protects against myocardial ischemia/reperfusion injury via inhibition of NF-κB signaling

Myocardial ischemia/reperfusion injury (MI/RI) following cardiac surgery is a leading cause of morbidity and mortality worldwide. The aim of the present study was to investigate the role of long non-coding RNA hypoxia/reoxygenation injury-related factor in myocytes (HRIM) on cardiac function following MI/RI. After establishing an MI/RI model, hemodynamic indices were detected via transthoracic echocardiography. The proliferative and apoptotic capacities of H9C2 cells subjected to oxygen-glucose deprivation/reoxygenation were detected via Cell Counting Kit-8 assay and flow cytometry, respectively. TNF-alpha, IL-1 beta, IL-6, lactate dehydrogenase (LDH) and creatine kinase (CK) levels were measured via ELISA. The expression levels of NF-kappa B-associated proteins were detected via western blotting. The expression levels of HRIM were increased in the myocardial tissue of MI/RI rats and H9C2 cells. The infarct size was significantly increased following induction of MI/RI. Moreover, increased HRIM expression levels suppressed hemodynamics in MI/RI rats. Knockdown of HRIM increased cell proliferation and decreased apoptosis as well as the protein levels of phosphorylated (p)-NF-kappa B p65/NF-kappa B p65, p-IkB alpha/IkB alpha, TNF-alpha, IL-1 beta, IL-6, LDH and CK in H9C2 cells; however, these effects were attenuated via activation of NF-kappa B signaling. Silencing of HRIM ameliorated MI/RI injury and alleviated inflammation via inactivating the NF-kappa B signaling pathway.