6.2 Neuroprotective effects of hydrogen sulfide
Ischemia-reperfusion injury of the brain is an important cause of ischemic stroke, mainly manifested by necrosis or softening of ischemic brain tissue and focal neuronal damage[130, 131]. Stroke is the most common cause of disability in developed countries, and its high morbidity and mortality pose a great threat to the health of the whole population[132, 133]Therefore, it is particularly important for researchers to find ways to detect and prevent ischemic strokes early. Fortunately, it has been found that appropriate concentrations of H2S have a neuroprotective effect in I/R injury in brain tissue[134, 135]. Many experimental data suggest that the use of H2S donors to provide low concentrations of H2S can reduce infarct size and restore neurological function in brain tissue through mechanisms such as antioxidant, anti-inflammatory, anti-apoptotic, modulation of autophagy, protection of mitochondrial function and vasodilation and vasogenesis[136-139]. In addition, it has been reported that H2S can also reduce infarct size and restore neurological function by modulating the expression of N-methyl-D-aspartate receptor (NMDA) receptor 的expression levels, thereby activating the CREB pathway and improving neuronal cell survival[140, 141].However, another study showed that high concentrations of hydrogen sulfide inhibited cytochrome C oxidase activity in experimental mice, leading to brainstem toxicity and respiratory depression[142].These suggest that H2S plays a dual biological role in the brain[143, 144] . Although the potential mechanisms of hydrogen sulfide in neuroprotection are still not well understood and refined, there is no doubt that as a multi-targeted neuromodulator, H2S has a very bright application in the treatment of ischemic stroke.
Figure 4