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