Hydrogen mediates suppression of colon inflammation induced by dextran sodium sulfate

By its antioxidant effect, molecular hydrogen gas (H2) was reported to protect organs from tissue damage induced by ischemia reperfusion. To evaluate its anti-inflammatory effects, we established a mouse model of human inflammatory bowel disease (IBD) by supplying mice with water containing (1) dextran sodium sulfate (DSS) (5%), (2) DSS (5%) and H2, or (3) H2 only ad libitum up to 7 days. At day-7, DSS-induced pathogenic outcomes including, loss of body weight, increase of colitis score, pathogenic shortening of colon length, elevated level of IL-12, TNF-alpha and IL-1beta in colon lesion, were significantly suppressed by the addition of H2 to DSS solution. Histological analysis also revealed that the DSS-mediated colonic tissue destruction accompanied by macrophage infiltration was remarkably suppressed by H2. Therefore, the present study indicated that H2 can prevent the development of DSS-induced colitis in mice.

Hydrogen from intestinal bacteria is protective for Concanavalin A-induced hepatitis

It is well known that some intestinal bacteria, such as Escherichia coli, can produce a remarkable amount of molecular hydrogen (H(2)). Although the antioxidant effects of H(2) are well documented, the present study examined whether H(2) released from intestinally colonized bacteria could affect Concanavalin A (ConA)-induced mouse hepatitis. Systemic antibiotics significantly decreased the level of H(2) in both liver and intestines along with suppression of intestinal bacteria. As determined by the levels of AST, ALT, TNF-alpha and IFN-gamma in serum, suppression of intestinal bacterial flora by antibiotics increased the severity of ConA-induced hepatitis, while reconstitution of intestinal flora with H(2)-producing E. coli, but not H(2)-deficient mutant E. coli, down-regulated the ConA-induced liver inflammation. Furthermore, in vitro production of both TNF-alpha and IFN-gamma by ConA-stimulated spleen lymphocytes was significantly inhibited by the introduction of H(2). These results indicate that H(2) released from intestinal bacteria can suppress inflammation induced in liver by ConA.