Protective effect of hydrogen sulfide on hypoxia-induced injury of rat cortical neurons

AIM:To explore the role of hydrogen sulfide (H 2S) in cortial neuronal injury induced by hypoxia.METHODS:The SD rat cortical neurons were cultured in hypoxic conditions (2% O 2, 5% CO 2 and 93% N 2 at 37 °C) to establish the hypoxic model. Sodium hydrosulfide (NaHS) was used as the donor of H 2S and neuronal viability was detected by CCK-8 assay. Neuronal content of reactive oxygen species (ROS) was determined by DCFH-DA method, and mitochondrial membrane potential (MMP) was detected using Rh123 staining. Lactate dehydrogenase (LDH) release rate was measured by a commercial kit to reflect the degree of neuronal injury. RESULTS:Hypoxic treatment increased ROS content and the release rate of LDH in the neurons. However, NaHS pretreatment significantly inhibited the hypoxia-induced increases in ROS content and LDH release. Hypoxia decreased MMP and cell viability. Pretreatment with NaHS and N-acetyl-L-cysteine (NAC), a ROS scavenger, significantly inhibited the decreases in MMP and viability of the neurons. CONCLUSION:Hypoxia induces ROS generation in the neurons, thereby decreases MMP and neuronal viability. H 2S significantly attenuates hypoxia-induced neuronal injury by its antioxygenation.