As an endogenous gas signalling molecule, hydrogen sulfide (H2S) is frequently present in a variety of mammals and plays a significant role in the cardiovascular and nervous systems. Reactive oxygen species (ROS) are produced in large quantities as a result of cerebral ischaemia-reperfusion, which is a very serious class of cerebrovascular diseases. ROS cause oxidative stress and induce specific gene expression that results in apoptosis. H2S reduces cerebral ischaemia-reperfusion-induced secondary injury via anti-oxidative stress injury, suppression of the inflammatory response, inhibition of apoptosis, attenuation of cerebrovascular endothelial cell injury, modulation of autophagy, and antagonism of P2X7 receptors, and it plays an important biological role in other cerebral ischaemic injury events. Despite the many limitations of the hydrogen sulfide therapy delivery strategy and the difficulty in controlling the ideal concentration, relevant experimental evidence demonstrating that H2S plays an excellent neuroprotective role in cerebral ischaemia-reperfusion injury (CIRI). This paper examines the synthesis and metabolism of the gas molecule H2S in the brain as well as the molecular mechanisms of H2S donors in cerebral ischaemia-reperfusion injury and possibly other unknown biological functions. With the active development in this field, it is expected that this review will assist researchers in their search for the potential value of hydrogen sulfide and provide new ideas for preclinical trials of exogenous H2S.
Keywords: Cerebral ischaemia-reperfusion injury; H(2)S donors; Hydrogen sulfide; Neuroprotective; Oxidative stress; P2X7 receptor.
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