Hydrogen Water Protects Joints from Arthritis Damage in Rats
- Authors
- ShaoWen Cheng, Lei Peng, BaiChao Xu, WenSheng Chen, YangPing Chen, YunTao Gu
- Journal
- Medical Science Monitor
- Year
- 2020
- DOI
- 10.12659/MSM.920211
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Osteoarthritis
- Body System
- Musculoskeletal
TL;DR
Drinking hydrogen-rich water helped reduce joint damage in rats with osteoarthritis by fighting oxidative stress and cartilage breakdown.
Key Finding
In a rat osteoarthritis model, hydrogen-rich water injected into the knee joint reduced cartilage damage by suppressing oxidative stress (cellular damage from harmful molecules) and preventing cartilage cell death.
Summary
Researchers gave rats with osteoarthritis (a joint disease involving cartilage breakdown) hydrogen-rich water injected directly into their knee joints. After two weeks of treatment, the hydrogen-rich water reduced damage to cartilage by decreasing harmful molecules called free radicals, slowing the release of cartilage-degrading enzymes, and preventing the death of cartilage cells.
Practical Takeaway
This is early-stage animal research only—it has not been tested in humans. The study injected hydrogen-rich water directly into the joint rather than testing drinking hydrogen water. While the results suggest hydrogen may have anti-inflammatory and protective properties in cartilage, much more research is needed before any conclusions can be drawn about whether hydrogen water might help with osteoarthritis in people.
Abstract
BACKGROUND The aim of this study was to investigate the mechanisms underlying the potential effects of hydrogen-rich water (HW) on articular cartilage in a rat osteoarthritis (OA) model. MATERIAL AND METHODS A rat model of OA was established using the modified Hulth method, and rats were forced to exercise for 30 min every day 1 week after surgery for 7 weeks. Mankin's method was used to score the severity of OA. The animals were assigned into the OA group, OA+HW group, and sham operation group. After 8 weeks, the animals in the OA group had a Mankin score >8 points, and HW was administered into the knee joint. After 2 weeks of treatment, articular cartilage was obtained for pathological examination, consisting of hematoxylin and eosin, toluidine blue, and Hoechst staining, as well as quantitative real-time PCR and Western blot analyses. This combination of pharmacological and molecular biological analyses was performed to examine the mechanism underlying the protective effect of HW on articular cartilage. RESULTS The antioxidant effects of HW suppressed oxidative damage, which may have aided the inhibition of ECM-degrading enzymes (MMP3, MMP13, ADAMT4, and ADAMT5), the upregulation of Col II and aggrecan expression, and the downregulation of COX-2, iNOS, and NO expression. The results of HE staining indicated intra-articular treatment of HW attenuated cartilage degradation. However, Hoechst staining in the OA group indicated the nuclei of the fragmented chondrocytes were condensed compared to the sham operation group, and this effect was inhibited by HW. CONCLUSIONS HW showed a protective effect against the progression of OA in an animal model, which may have been mediated by its anti-oxidant and anti-apoptotic activities.