Abstract
Accumulating evidence has suggested that hydrogen sulfide (H2S) is endogenously generated in many types of mammalian cells. Since H2S plays an important role in cardiovascular, central nervous and gastrointestinal systems, it is currently considered to be the third gaseous mediator. Recently, more and more attention has been paid to the biological functions of H2S in inflammation. In various animal models of inflammatory diseases (such as acute pancreatitis, sepsis and endotoxemia), endogenous H2S has been shown to be overproduced and participate in regulating the severity of inflammatory response and associated organ injury. Inhibition of H2S formation is likely to protect animals against these inflammatory diseases. H2S may exert its effect on inflammation via regulating the function of leukocytes, leukocyte trafficking and immune cell survival. Furthermore, H2S has been suggested to induce the release or production of neuropeptides (substance P and calcitonin gene-related peptide), which are considered to be pro-inflammatory mediators, and therefore contribute to inflammatory response. In addition, some studies reported that low doses of sodium hydrosulfide (NaHS, an H2S donor) exhibited some anti-inflammatory effect on local inflammation (such as non-steroidal anti-inflammatory drug-induced gastric injury). Taken together, all these findings demonstrate that in addition to the vasodilation and neuromodulation activity of H2S, it may contribute to the pathogenesis of inflammatory diseases via regulating the activation of leukocytes.