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‑α, IL‑1β, IL‑6, lactate dehydrogenase (LDH) and creatine kinase (CK) levels were measured via ELISA. The expression levels of NF‑κB‑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‑κB p65/NF‑κB p65, p‑IkBα/IkBα, TNF‑α, IL‑1β, IL‑6, LDH and CK in H9C2 cells; however, these effects were attenuated via activation of NF‑κB signaling. Silencing of HRIM ameliorated MI/RI injury and alleviated inflammation via inactivating the NF‑κB signaling pathway.