Hydrogen Water Reduces Gut Inflammation in Ulcerative Colitis Study
- Authors
- Tao Yang, Futai Lu, Yumei Kang, Lei Wang, Man Li, Wenxue Xu, Sisi Bai, Yonghao Yu, Yang Shi, Hai Qin
- Journal
- International Immunopharmacology
- Year
- 2026
- DOI
- 10.1016/j.intimp.2026.116726
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Ulcerative Colitis
- Body System
- Digestive
TL;DR
Molecular hydrogen reduced ulcerative colitis–like inflammation and tissue injury in cell and mouse models by promoting PKM2 lactylation, which restrained NLRP3 inflammasome activation, pyroptosis, and inflammatory cytokine release.
Key Finding
Molecular hydrogen reduced inflammation and cell damage in ulcerative colitis models by promoting a chemical modification of the PKM2 protein, which then blocked activation of the NLRP3 inflammasome—a key driver of gut inflammation.
Summary
This study investigated how molecular hydrogen might help treat ulcerative colitis (a chronic inflammatory bowel disease) by examining its effects on cells and mice. Researchers found that hydrogen-rich water and hydrogen-rich medium reduced inflammation, cell damage, and a type of cell death called pyroptosis by activating a protein called PKM2, which then blocked an inflammation-triggering system called the NLRP3 inflammasome.
Practical Takeaway
While this research identifies a promising mechanism by which hydrogen might help ulcerative colitis, the study was conducted only in laboratory cells and mice, not in humans. These early findings suggest hydrogen may warrant further investigation, but much more research—including human clinical trials—would be needed before any health recommendations could be made.
Abstract
Background: Molecular hydrogen is considered to be able to alleviate the progression of ulcerative colitis (UC), whose underlying molecular mechanism remains largely unclear. Methods: Lipopolysaccharide (LPS)/adenosine triphosphate (ATP)-stimulated human colonic epithelial cells (HCoEpiC) were used to mimic UC model in vitro and were treated with hydrogen-rich medium (HRM). Dextran sulfate sodium (DSS)-induced mice were used to construct UC model in vivo and were administrated by hydrogen-rich water (HRW). Colon tissues from UC patients and healthy volunteers were collected. Release of inflammatory cytokines was detected by ELISA. Cell viability, gut pathological impairment and pyroptosis were assessed by CCK-8 assay, HE staining and transmission electron microscope (TEM). The protein expressions of NLRP3 inflammasome and pyruvate kinase M2 (PKM2) were analyzed by western blot. The interaction between NLRP3 and PKM2 was verified by co-immunoprecipitation (Co-IP) assay. Results: Molecular hydrogen alleviated cell viability inhibition and cytokines production in HCoEpiC cells, and suppressed gut injury, inflammation, pyroptosis and NLRP3 inflammasome activation in mice. PKM2 lactylation was down-regulated in colon tissues of UC patients. Molecular hydrogen treatment promoted PKM2 lactylation without affecting total PKM2 expression. The lactylation inhibitor, sodium oxamate, abolished molecular hydrogen-mediated protective effects on UC. Additionally, molecular hydrogen facilitated the combination between PKM2 and NLRP3 to down-regulate inflammasome activation. This binding between PKM2 and NLRP3 was abolished by disrupting PKM2 lactylation. Furthermore, the structural interaction between lactylated PKM2 and NLRP3 was predicted. Conclusion: Molecular hydrogen can promote PKM2 lactylation to restrain NLRP3 inflammasome-mediated pyroptosis and inflammation, thus ameliorating UC progression.