Hydrogen Water May Protect Joint Cartilage by Blocking Harmful Cell Signals
- Authors
- Yingni Lin, Bisei Ohkawara, Mikako Ito, Nobuaki Misawa, Kentaro Miyamoto, Yasuhiko Takegami, Akio Masuda, Shinya Toyokuni, Kinji Ohno
- Journal
- Scientific Reports
- Year
- 2016
- DOI
- 10.1038/srep31986
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Osteoarthritis
- Body System
- Musculoskeletal
TL;DR
Hydrogen gas helps to control a specific cell signaling pathway that is linked to various diseases, potentially explaining its protective effects.
Key Finding
Molecular hydrogen suppresses an overactive cellular signaling pathway (Wnt/β-catenin) by promoting the breakdown of a key protein called β-catenin, and this effect was observed in both laboratory cells and in rats with osteoarthritis.
Summary
Researchers discovered that molecular hydrogen (H2) works by turning off an overactive cellular signaling pathway called Wnt/β-catenin, which is involved in several diseases. In laboratory cells and in rats with osteoarthritis (joint damage), hydrogen water appeared to reduce cartilage breakdown by suppressing this pathway. The study identified the specific molecular steps involved in how hydrogen produces this effect.
Practical Takeaway
This early laboratory and animal study suggests a potential mechanism by which hydrogen water might help with osteoarthritis and other conditions involving abnormal Wnt/β-catenin signaling. However, these findings are from cell cultures and rats, not humans, so it remains unclear whether the same effects would occur in people. More research in human subjects would be needed before drawing any conclusions about hydrogen water's therapeutic value.
Abstract
Molecular hydrogen (H2) is effective for many diseases. However, molecular bases of H2 have not been fully elucidated. Cumulative evidence indicates that H2 acts as a gaseous signal modulator. We found that H2 suppresses activated Wnt/β-catenin signaling by promoting phosphorylation and degradation οf β-catenin. Either complete inhibition of GSK3 or mutations at CK1- and GSK3-phosphorylation sites of β-catenin abolished the suppressive effect of H2. H2 did not increase GSK3-mediated phosphorylation of glycogen synthase, indicating that H2 has no direct effect on GSK3 itself. Knock-down of adenomatous polyposis coli (APC) or Axin1, which form the β-catenin degradation complex, minimized the suppressive effect of H2 on β-catenin accumulation. Accordingly, the effect of H2 requires CK1/GSK3-phosphorylation sites of β-catenin, as well as the β-catenin degradation complex comprised of CK1, GSK3, APC, and Axin1. We additionally found that H2 reduces the activation of Wnt/β-catenin signaling in human osteoarthritis chondrocytes. Oral intake of H2 water tended to ameliorate cartilage degradation in a surgery-induced rat osteoarthritis model through attenuating β-catenin accumulation. We first demonstrate that H2 suppresses abnormally activated Wnt/β-catenin signaling, which accounts for the protective roles of H2 in a fraction of diseases.