Hydrogen sulphide protects H9c2 cells against chemical hypoxia-induced injury

P>1. The aim of the present study was to investigate the effect of hydrogen sulphide (H2S) on cobalt chloride (CoCl2)-induced injury in H9c2 embryonic rat cardiac cells. 2. After 36 h incubation in the presence of 600 mu mol/L CoCl2, reduced cell viability of H9c2 cells was observed, as well as the induction of apoptosis. In addition, CoCl2 (600 mu mol/L) enhanced the production of reactive oxygen species (ROS) and the expression of cleaved caspase 3, induced a loss of mitochondrial membrane potential (MMP) and decreased reduced glutathione (GSH) production. These results suggest that CoCl2 induces similar responses to hypoxia/ischaemia. 3. Pretreatment of cells with 400 mu mol/L NaHS (a H2S donor) for 30 min prior to exposure to CoCl2 (600 mu mol/L) significantly protected H9c2 cells against CoCl2-induced injury. Specifically, increased cell viability and decreased apoptosis were observed. In addition, NaHS pretreatment blocked the CoCl2-induced increases in ROS production and cleaved caspase 3 expression, as well as the decreases in GSH production and loss of MMP. 4. Pretreatment of cells with 2000 mu mol/L N-acetylcysteine (NAC), a ROS scavenger, for 1 h prior to CoCl2 exposure significantly protected H9c2 cells against CoCl2-induced injury, specifically enhancing cell viability, decreasing ROS production and preventing loss of MMP. 5. The findings of the present study suggest that H2S protects H9c2 cells against CoCl2-induced injury by suppressing oxidative stress and caspase 3 activation.