5.4 Inflammation
During reperfusion, the production of a large amount of ROS activates the NF-κB gene, further stimulating the secretion of TNF-α by endothelial cells and macrophages[104]. On the one hand, TNF-α can induce cell apoptosis through sphingosine dependent mechanism. On the other hand, it can also cause leukocyte infiltration in damaged tissues, increase the permeability of vascular endothelial cells, produce no reflow phenomenon, and aggravate reperfusion injury[105, 106]. At the same time, activated cells release a large amount of inflammatory factors, such as IL-1, IL-6, IL-8, IL-10, IL-18, etc[107].
H2S and I/R injury6.1 Myocardial protective effect of H2S
When the blood perfusion and oxygen supply of the myocardium are severely reduced, extensive cell death may occur, leading to myocardial infarction[108, 109]. As mentioned earlier, although restoring blood supply can alleviate ischemia to a certain extent, it can also lead to a series of more serious reactions, such as oxidative stress, cell damage, and even death. In current research on I/R, increasing evidence suggests that endogenous H2S regulation or exogenous H2S donors may be involved in the pathogenesis of ischemic cardiomyopathy, improving cardiac function, controlling structural lesions, and reducing related complications[110-112]. We found that H2S may have a protective effect on myocardial cells through the following five mechanisms.