H2O2 evokes injury of cardiomyocytes through upregulating HMGB1

Reactive oxygen species (ROS) have been shown to induce cell apoptosis in cardiomyocytes. However, the underlying mechanism remains unclear. This study aimed to investigate the role of high-mobility group box 1 protein (HMGB1) in cardiomyocytes undergoing H2O2 treatment.

Neonatal rat cardiomyocytes were treated with H2O2 (100, 200, 500 µM) or pre-treated with antioxidant N-acetylcysteine (NAC 200 µM) or HMGB1 neutralizing antibody (20 µg/ml) in an appropriate concentration of H2O2 (200 µM). The cell viability, apoptosis rate, lactate dehydrogenase (LDH), and the activity of superoxide dismutase were measured. HMGB1 expression was assessed by immunoblotting.

H2O2-induced ROS significantly decreased cell viability, promoted the apoptosis of neonatal myocytes, and upregulated the expression of HMGB1 in a dose-dependent manner. However, NAC or HMGB1 neutralizing antibody suppressed the loss of cell viability and the rate of cell apoptosis induced by H2O2. NAC or HMGB1 neutralizing antibody also significantly suppressed the release of LDH and the expression of HMGB1.

The present study suggests that H2O2-induced ROS evoke injury to cardiomyocytes that may be associated with upregulating HMGB1.