Minocycline relieves myocardial ischemia-reperfusion injury in rats by inhibiting inflammation, oxidative stress and apoptosis.

Abstract

Myocardial ischemia-reperfusion (I/R) injury (MIRI) is an important cause of irreversible injury to the myocardium in patients with acute myocardial infarction. The purpose of this study was to investigate the effects of minocycline (MC) on inflammation, oxidative stress and apoptosis of myocardial tissues. We used rats to establish MIRI model by ligating coronary arteries. The structure and function of rat myocardium were determined by 2, 3, 5-triphenyl tetrazolium chloride (TTC) staining, hematoxylin-eosin (HE) staining and echocardiography. In addition, we detected the expression of inflammatory factors, antioxidant enzymes and apoptosis-related molecules in rats by enzyme-linked immunosorbent assay (ELISA), immunohistochemical (IHC) staining and reverse transcription-polymerase chain reaction (RT-PCR) to determine the effect of MC on inflammation, oxidative stress and apoptosis in I/R rats. Finally, we studied the effect of MC stimulation on the viability of rat cardiomyocytes (H9c2 cells) in vitro. After I/R, the heart function of rats decreased, and the structure of myocardium was destroyed. The levels of inflammation and oxidative stress in I/R rats also increased significantly, manifested by increased inflammatory factors and decreased antioxidant enzymes in serum and myocardial tissue. After treatment of I/R rats with MC, the structure and function of rat myocardium improved significantly, and MC reduced inflammation and oxidative stress levels in rats, thus inhibiting the apoptosis of cardiomyocytes. MC also improved the viability of H9c2 cells in vitro. MC reduced inflammation and oxidative stress levels in MIRI rat model or H9c2 cells, thus inhibiting cardiomyocyte apoptosis. Therefore, MC has potential application prospects for the treatment of MIRI.