Hydrogen sulfide prevents OGD/R-induced apoptosis via improving mitochondrial dysfunction and suppressing an ROS-mediated caspase-3 pathway in cortical neurons.

Hydrogen sulfide (H2S), an endogenous gaseous mediator, has been shown to have protective effects against neuronal damage caused by brain ischemia. In this study, we explored the potential effects of H2S on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced neuronal apoptosis and the possible mechanisms. We find that sodium hydrosulfide (NaHS, a donator of H2S) prevents OGD/R-induced intracellular reactive oxygen species (ROS) elevation and activation of caspase-3 in cultured mouse cortical neurons.

Hydrogen sulfide prevents hypoxia-induced apoptosis via inhibition of an H2O2-activated calcium signaling pathway in mouse hippocampal neurons.

Hydrogen sulfide (H(2)S), an endogenous gaseous mediator, has been shown to exert protective effects against damage to different organs in the human body caused by various stimuli. However, the potential effects of H(2)S on hypoxia-induced neuronal apoptosis and its mechanisms remain unclear. Here, we exposed mouse hippocampal neurons to hypoxic conditions (2% O(2), 5% CO(2) and 93% N(2) at 37 °C) to establish a hypoxic cell model.