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.