Attenuating Ischemia-Induced H9c2 Myoblasts Apoptosis by Therapeutic Hypothermia

Although inducing mild hypothermia (32 °C) in animal models of cardiac arrest with highly attenuated cardiac and neurological injury, the protective effects of hypothermia molecular mechanisms were not fully elucidated, and thus, were examined here on the H9c2 rat ventricular myoblasts that underwent cell loss as well as apoptosis in conditions of simulated ischemia, represented by serum withdrawal plus hypoxia. The H9c2 cells apoptosis was evidenced by flow cytometry-, DNA fragmentation-, and caspase 3 activation-increased apoptotic cells (Annexin-V positive and propidium iodide negative). For the simulated ischemia, both cell loss and apoptosis of these cardiomyoblasts were associated with downregulated small molecular weight proteins (heat shock protein 20, heat shock protein 27, and αB-crystallin). Mild hypothermia significantly reduced the ischemia-induced apoptosis, small molecular weight proteins downregulation, and cell viability cut. Conclusively, hypothermia may inhibit simulated ischemia-induced apoptosis in cardiomyocytes by restoring normal small molecular weight proteins expression.