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].