Silencing of long non­coding RNA HRIM protects against myocardial ischemia/reperfusion injury via inhibition of NF­κB 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 non­coding RNA hypoxia/reoxygenation injury­related 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 oxygen­glucose deprivation/reoxygenation were detected via Cell Counting Kit­8 assay and flow cytometry, respectively. TNF­α, IL­1ß, IL­6, lactate dehydrogenase (LDH) and creatine kinase (CK) levels were measured via ELISA. The expression levels of NF­κB­associated 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)­NF­κB p65/NF­κB p65, p­IkBα/IkBα, TNF­α, IL­1ß, IL­6, LDH and CK in H9C2 cells; however, these effects were attenuated via activation of NF­κB signaling. Silencing of HRIM ameliorated MI/RI injury and alleviated inflammation via inactivating the NF­κB signaling pathway.