Exogenous H2S promotes ion channel reconstruction to regulate colonic motility in rats with dinitrobenzene sulfonic acid-induced colitis.

Background: Hydrogen sulfide (H2S) is a newly recognized endogenously generated gasotransmitter. Endogenous H2S has been shown to be related to several gastrointestinal diseases, including irritable bowel syndrome, Crohn's disease, and ulcerative colitis. We explored the functional role of H2S in colitis and investigated the underlying mechanism.

Exogenous HS Protects Colon Cells in Ulcerative Colitis by Inhibiting and Activating Autophagy.

Hydrogen sulfide (HS) has been reported to participate in intestinal mucosal defense and repair. However, the precise regulatory mechanisms of HS in ulcerative colitis (UC) remain unclear. We explored the effects of sodium hydrosulfide (NaHS), a donor of HS, in dextran sulfate sodium (DSS)-induced colitis in rats.

Release of endogenous hydrogen sulfide in enteric nerve cells suppresses intestinal motility during severe acute pancreatitis.

Previous studies have shown that during severe acute pancreatitis (SAP) attacks, hydrogen sulfide (H2S) is released in the colon. However, the roles played by H2S in regulating enteric nerves remain unclear. In this study, we examined the association between SAP-induced H2S release and loss of intestinal motility, and also explored the relevant mechanism in enteric nerve cells.

Curcumin regulates the miR-21/PTEN/Akt pathway and acts in synergy with PD98059 to induce apoptosis of human gastric cancer MGC-803 cells.

Objective: PD98059 is a potent and selective inhibitor of mitogen-activated protein kinase. Substantial preclinical evidence has shown an anti-tumor effect of curcumin on various solid tumors. This study aimed to investigate whether curcumin synergistically acts with PD98059 in exerting anti-gastric cancer effects.

Pro-inflammatory cytokine-driven PI3K/Akt/Sp1 signalling and HS production facilitates the pathogenesis of severe acute pancreatitis.

Severe acute pancreatitis (SAP) is a disease usually associated with systemic organ dysfunction or pancreatic necrosis. Most patients with SAP suffer from defective intestinal motility in the early phase of the disease. Additionally, SAP-induced inflammation produces hydrogen sulphide (HS) that impairs the gastrointestinal (GI) system.