Hydrogen sulfide protects H9c2 cardiomyoblasts against H(2)O(2)-induced apoptosis

Reactive oxygen species (ROS) are highly reactive chemical species that may cause irreversible tissue damage, and play a critical role in cardiovascular diseases. Hydrogen sulfide (H(2)S) is a gasotransmitter that acts as a ROS scavenger with cardio-protective effects. In this study, we investigated the cytoprotective effect of H(2)S against H(2)O(2)-induced apoptosis in cardiomyocytes. H9c2 rat cardiomyoblasts were treated with H(2)S (100 μM) 24 h before challenging with H(2)O(2) (100 μM). Apoptosis was then assessed by annexin V and PI, and mitochondrial membrane potential was measured using a fluorescent probe, JC-1. Our results revealed that H(2)S improved cell viability, reduced the apoptotic rate, and preserved mitochondrial membrane potential. An increased Bcl-2 to Bax ratio was also seen in myocytes treated with H(2)S after H(2)O(2)-induced stress. Our findings indicated a therapeutic potential for H(2)S in preventing myocyte death following ischemia/reperfusion.