Hydrogen Sulfide in Airway Diseases.
Although the anti-inflammatory mechanism of H2S is not clear, the exogenous addition of H2S could inhibit Th2-cytokines like IL-5 and IL-13 in addition toeotaxin-1 in the BAL fluid in an OVA-induced murine asthma model.
H2S can freely cross the plasma membrane and the mitochondrial membrane to scavenge Reactive Oxygen Species and Reactive Nitrogen Species. Moreover, H2S enhances the production of reduced Glutathione by enhancing cystine/cysteine transporters and redistributes GSH to mitochondria.
NaHS increased the ratio of reduced/oxidized glutathione and decreased the content of 8-hydroxy-deoxyguanosine in the lungs of CS-exposed mice,10 which was similar to our findings that NaHS inhibited ozone-induced oxidative stress in a murine model.
Benetti, et al confirmed that NaHS treatment abolished the increased lipid peroxidation in the allergic mouse lungs and increased Superoxide dismutase, Glutathione peroxidase and Glutathione Reductase enzyme activities. Nuclear factor-like 2, also known as Nrf2, is a key transcription factor that regulates the expression of many important antioxidant proteins that protect against oxidative damage triggered by injury and inflammation.
H2S can inhibit cell proliferation; however, the effects of H2S on cellular apoptosis are complex. An in vitro study showed that both NaHS and GYY4137 suppressed human Airway Smooth Muscle Cell proliferation induced by Fetal Bovine Serum and the proinflammatory cytokines IL-1β and IL-8. H2S decreased the migration and proliferation of a human lung fibroblast cell line stimulated by FBS and basic Fibroblast Growth Factor, which is probably related to the fact that H2S inhibits ERK-1/2 phosphorylation in MRC5 cells.
Pulm Res Respir Med Open J. 2015; 2(2): 81-83. doi: 10.17140/PRRMOJ-2-113
