H2-rich water reduces inflammation and oxidative stress in colitis miceScientific Research

original title: Hydrogen-rich water partially alleviate inflammation, oxidative stress and intestinal flora dysbiosis in DSS-induced chronic ulcerative colitis mice


Lihua Song, Yao Zhang, Chuang Zhu, Xinwen Ding, Li Yang, Hongli Yan

DOI: 10.1016/j.advms.2021.10.002



Purpose: Oxidative damage and intestinal flora dysbiosis play important roles in the progression of chronic ulcerative colitis (UC). This study explored the effect and mechanism of molecular hydrogen in chronic UC.

Materials and methods: Male C57BL/6 mice (19.6 ​± ​0.4 ​g, 7 weeks) were randomly divided into 3 groups: normal control (NC) group, UC (Dextran Sulfate Sodium, DSS) group, and hydrogen-rich water (HRW, 0.8 ​ppm)-treated UC (DSS ​+ ​HRW) group. Mice in the DSS treatment group were treated with DSS for the following 3 cycles to establish chronic UC model: the first 2 cycles consisted of 2.5% DSS for 5 days, followed by drinking water for 16 days, and a third cycle consisted of 2% DSS for 4 days, followed by drinking water for 10 days. The mice in the DSS ​+ ​HRW group were administered HRW daily throughout the experiment.

Results: The mice in the DSS groups developed typical clinical signs of colitis. HRW treatment partially ameliorated colitis symptoms, improved histopathological changes, significantly increased glutathione (GSH) concentration and decreased TNF-α level. Notably, HRW treatment significantly inhibited the growth of Enterococcus faecalis, Clostridium perfringens and Bacteroides fragilis (P ​< ​0.05 vs. DSS group), with the relative abundance that was close to the levels in the NC group. Microarray analysis revealed that 252 genes were significantly modified after HRW treatment compared with those in the DSS treatment alone group, and 17 genes were related to inflammation, including 9 interferon-stimulated genes (ISGs). Conclusions: Hydrogen-rich water partially alleviates inflammation, oxidative stress and intestinal flora dysbiosis in DSS-induced chronic UC mice.