• Inhibition of H₂S caused deterioration of DSS-induced colitis and H₂S might act as an anti-inflammatory molecule in mouse colitis.1
  • Inhibition of colonic H₂S markedly exacerbated the colitis, resulting in significant mortality. Inhibition of H₂S synthesis in healthy rats resulted in inflammation and mucosal injury in the small intestine. Intracolonic administration of H₂S significantly reduced the severity of colitis and inflammation. ATB-429, a H₂S -releasing mesalamine derivative, reduces colitis-associated leukocyte infiltration and the expression of pro-inflammatory cytokines in the mouse colon3,4
  • Administration H₂S donor to Hhcy Il-10 deficient rats significantly decreased the severity of colitis and IL-10 contributed to H₂S dysregulation5
  • There is an upregulation of H₂S to heal mucosal tissue in colitis but an inactivation of H₂S at the site of ulceration6

  • Endogenous H₂S anion secretion was reduced in colitis model indicating a desensitization of the tissue by inflammation, which might be explained by an upregulation of colonic H₂S production as described in some models of inflammation7
  • Luminal H₂S causes excitation of sensory nerves most probably by activating Ca(v)3.2 T-type Ca(2+) channels that are upregulated in the early stage of colitis, leading to colonic mucosal cytoprotection in rats8
  • Exacerbation of colitis in Hhcy is due in part to impaired colonic H2S synthesis. Moreover, IL-10 plays a novel role in promoting H2S production and homocysteine metabolism, which may have therapeutic value in conditions characterized by Hhcy9
  • H2S successfully rescues epithelial cell damage induced by oxidative stress in vitro. This indicates that H2S could be a potential pharmacological intervention in conditions like necrotizing enterocolitis.10