Abstract
The brain is the most sensitive organ to hypoxia in the human body. Hypoxia in the brain will lead to damage to local brain tissue. When the blood supply of ischemic brain tissue is restored, the damage will worsen, that is, cerebral ischemia-reperfusion injury. Hydrogen sulfide (H(2)S) is a gaseous signal molecule and a novel endogenous neuroregulator. Indeed, different concentrations of H(2)S have different effects on neurons. Low concentration of H(2)S can play an important protective role in cerebral ischemia-reperfusion injury by inducing anti-oxidative stress injury, inhibition of inflammatory response, inhibition of cell apoptosis, reduction of cerebrovascular endothelial cell injury, regulation of autophagy, and other ways, which provides a new idea for clinical diagnosis and treatment of related diseases. This review aims to report the recent research progress on the dual effect of H(2)S on brain tissue during cerebral ischemia/reperfusion injury.