Hydrogen Water Reduces Inflammation and Arthritis in Lab Study

Authors
Journal
Biochemical and Biophysical Research Communications
Year
DOI
10.1016/j.bbrc.2011.06.116
Study Type
Cell Culture
Outcome
Positive
Peer Reviewed
Yes
Country
Japan
Health Condition
Rheumatoid Arthritis
Body System
Immune System

TL;DR

Molecular hydrogen can reduce inflammation and help with arthritis by affecting cell signaling without changing oxidative stress levels.

Key Finding

Molecular hydrogen reduced inflammatory nitric oxide production in immune cells by blocking specific cell signaling pathways, not through direct antioxidant effects.

Summary

Researchers studied how molecular hydrogen affects inflammation in immune cells called macrophages. They found that hydrogen reduced the production of nitric oxide (a signaling molecule involved in inflammation) by blocking specific cellular communication pathways, rather than simply acting as an antioxidant. When mice with an arthritis-like condition drank hydrogen-rich water, their symptoms improved, suggesting hydrogen may help reduce inflammatory diseases.

Practical Takeaway

This laboratory and animal study suggests hydrogen may modulate inflammation through a novel mechanism involving cell signaling rather than oxidative stress reduction. However, these findings are from cell cultures and mice only; human studies would be needed to determine if hydrogen-rich water has similar anti-inflammatory effects in people with arthritis or other inflammatory conditions.

Abstract

Molecular hydrogen has been reported to be effective for a variety of disorders and its effects have been ascribed to the reduction of oxidative stress. However, we have recently demonstrated that hydrogen inhibits type I allergy through modulating intracellular signal transduction. In the present study, we examined the hydrogen effects on lipopolysaccharide/interferon γ LPS/IFNγ-induced nitric oxide (NO) production in murine macrophage RAW264 cells. Treatment with hydrogen reduced LPS/IFNγ-induced NO release, which was associated with a diminished induction of inducible isoform of nitric oxide synthase (iNOS). Hydrogen treatment inhibited LPS/IFNγ-induced phosphorylation of apoptosis signal-regulating kinase 1 (ASK1) and its downstream signaling molecules, p38 MAP kinase and JNK, as well as IκBα, but did not affect activation of NADPH oxidase and production of reactive oxygen species (ROS). As ROS is an upstream activator of ASK1, inhibition of ASK1 by hydrogen without suppressing ROS implies that a potential target molecule of hydrogen should be located at the receptor or immediately downstream of it. These results suggested a role for molecular hydrogen as a signal modulator. Finally, oral intake of hydrogen-rich water alleviated anti-type II collagen antibody-induced arthritis in mice, a model for human rheumatoid arthritis. Taken together, our studies indicate that hydrogen inhibits LPS/IFNγ-induced NO production through modulation of signal transduction in macrophages and ameliorates inflammatory arthritis in mice, providing the molecular basis for hydrogen effects on inflammation and a functional interaction between two gaseous signaling molecules, NO and molecular hydrogen.