| First Author | Qin M | Year | 2019 |
| Journal | Free Radic Biol Med | Volume | 137 |
| Pages | 99-109 | PubMed ID | 31026586 |
| Mgi Jnum | J:295527 | Mgi Id | MGI:6453922 |
| Doi | 10.1016/j.freeradbiomed.2019.04.025 | Citation | Qin M, et al. (2019) Hydrogen sulfide protects against DSS-induced colitis by inhibiting NLRP3 inflammasome. Free Radic Biol Med 137:99-109 |
| abstractText | Hydrogen sulfide (H2S), as the third gasotransmitter, has been shown to be effective in the prevention of inflammation. In addition, the NLRP3 inflammasome is a key player in the pathogenesis of dextran sulfate sodium (DSS)-induced colitis. Therefore, the aim of our research was to determine whether H2S exerts an anti-inflammatory effect on DSS-induced colitis by targeting NLRP3 inflammasome. Our data showed that DSS-induced colitis is attenuated by H2S, lessening the shortening of the colon lengths and colonic pathological damages. The cytokines TNF-alpha, IL-1beta, and IL-6 in colon samples were also significantly downregulated by H2S. Besides, H2S markedly suppressed the expression of NLRP3 and cleaved caspase-1 (p20) in colons from DSS-induced colitis mice. More importantly, CSE(-/-) mice were more susceptive to DSS-induced colitis when compared to wild-type (WT) mice. Our experimental results also suggested that H2S dose-dependently inhibits the activation of NLRP3 inflammasome in bone marrow-derived macrophages (BMDMs) by reducing the cleavage of caspase-1 and the secretion of IL-1beta. Furthermore, the inhibitory effect of H2S is due to a reduction in reactive oxygen species (ROS) generation and partly dependent on the disruption of nuclear erythroid 2-related factor-2 (Nrf2) activation. Collectively, our study confirms that H2S exerts its protective effect on DSS-induced mouse colitis at least partly by inhibiting the activation of NLRP3 inflammasome pathway. |
