6.1.4 Inhibition of inflammation
In the current study, hydrogen sulfide can inhibit the inflammatory
response of cardiomyocytes, which is one of the important mechanisms for
its cardioprotective effect[120, 121]. In earlier
years, some researchers found that certain H2S donors
can reduce leukocyte adhesion and infiltration, and this effect seems to
be related to the activation of KATPchannels[122, 123]. In addition to this,
administration of H2S treatment before the ischemic
tissue regains blood supply also prevents the activation of NF-κB and
reduces the production of pro-inflammatory mediators, with the most
significant reduction of IL-1 and IL-6[124, 125].
Increased expression levels of TNF-α during reperfusion promote
interaction between leukocytes and endothelial cells, resulting in
increased infiltration of inflammatory cells in the I/R region of the
myocardium, which leads to more severe myocardial injury, so inhibition
of TNF-α expression may attenuate myocardial injury. It has been found
that H2S can inhibit the adhesion of inflammatory cells
and the release of associated inflammatory factors caused by TNF-α
activation, significantly reducing the expression levels of chemotactic
protein-1 (MCP-1), adhesion factors, etc[126].