Therapeutic Effects of Hydrogen Sulfide in Treating Delayed Encephalopathy After Acute Carbon Monoxide Poisoning

Carbon monoxide (CO) poisoning is one of the most common diseases induced by CO injury. More than a half of the survivors still likely to have cognitive dysfunction, which is delayed encephalopathy after acute CO poisoning. There is no other effective treatment for delayed encephalopathy after acute CO poisoning except hyperbaric oxygen. Hydrogen sulfide is a novel signal molecule for the central nervous system regulation and plays a role of neural protection in many diseases. H2S has the inhibitory effects on oxidative stress and apoptosis to protect against oxidative damage of nerve. A CO-poisoning rat model was established to detect the effect of H2S on delayed encephalopathy after acute CO poisoning. Spatial learning and memory was tested by Morris water maze. Nissl staining and terminal deoxynucleotidyl transferase-mediated nick end labeling assay were used to examine apoptosis induced by CO poisoning in the brain. Then, the protein levels of proinflammatory cytokines and the indicators of oxidative damage were measured. We found that H2S significantly improved cognitive function, reduced apoptosis and the inflammatory response, and decreased the oxidative damage induced by CO poisoning in rats. These results suggest that H2S may be a novel specific and effective treatment of delayed encephalopathy of CO poisoning.