Hydrogen from intestinal bacteria is protective for Concanavalin A-induced hepatitis.
Mikihito Kajiya, Kimihiro Sato, Marcelo J B Silva, Kazuhisa Ouhara, Phi M Do, K T Shanmugam, Toshihisa Kawai · Biochemical and biophysical research communications · 2009
Research-use notice
Independent study record
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H2HUBB TAKEAWAY
In vitro production of both TNF-alpha and IFN-gamma by ConA-stimulated spleen lymphocytes was significantly inhibited by the introduction of H(2), systemic antibiotics significantly decreased the level of H(2) in both liver and intestines along with suppression of intestinal bacteria. These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.
What the Researchers Tested
In vitro production of both TNF-alpha and IFN-gamma by ConA-stimulated spleen lymphocytes was significantly inhibited by the introduction of H(2).
How Molecular Hydrogen Was Used
The source material available to H2HUBB did not provide enough detail to identify the molecular hydrogen administration method.
Laboratory Model
In vitro production of both TNF-alpha and IFN-gamma by ConA-stimulated spleen lymphocytes was significantly inhibited by the introduction of H(2).
What Molecular Hydrogen Changed
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.
H₂ Mechanisms / Biological Findings
The source material reviewed did not establish a specific molecular hydrogen mechanism for the reported findings.
Authors’ Conclusion
The authors concluded that these results indicate that H(2) released from intestinal bacteria can suppress inflammation induced in liver by ConA.