Hydrogen Therapy Shows Promise for Treating Arthritis Joint Pain
- Authors
- Hongwei Lu, Wei Wang, Xiaodiao Kang, Zeng Lin, Jun Pan, Shaowen Cheng, Jingdong Zhang
- Journal
- Journal of Inflammation Research
- Year
- 2021
- DOI
- 10.2147/JIR.S297622
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Osteoarthritis
- Body System
- Musculoskeletal
TL;DR
Hydrogen gas treatment may help protect against the damage and inflammation seen in osteoarthritis by blocking a specific signaling pathway in cells.
Key Finding
Hydrogen gas reduced cartilage cell death and inflammatory damage in both laboratory cells and mice with surgically-induced osteoarthritis by blocking the JNK signaling pathway.
Summary
Researchers tested whether hydrogen gas could help protect against osteoarthritis (a disease where joint cartilage breaks down) by studying its effects on cartilage cells and in mice with artificially induced joint damage. They found that hydrogen reduced both cell death and inflammatory molecules that damage cartilage, and these effects appeared to work by blocking a specific cellular signaling pathway called JNK.
Practical Takeaway
While these results are promising, this research was conducted only in mice and laboratory cells—not in humans. Early evidence suggests hydrogen may help slow osteoarthritis progression, but human studies would be needed to determine whether hydrogen water or gas could provide similar benefits for people with joint disease.
Abstract
Background: Osteoarthritis (OA) is a very common condition and leads to joint pain, disability, and price tag all over the world. Pathogenesis of OA is closely related to numerous inflammatory and apoptosis cytokines. Hydrogen (H2) reportedly exhibits a diversity of effects such as anti-apoptotic, anti-inflammatory, and anti-oxidative properties via the JNK pathway. However, it is unknown whether H2 has a protective effect against OA via the JNK signaling pathway. Therefore, the aim of this study was to figure out whether hydrogen has protective effect on chondrocyte and further explore the possible underlying mechanism. Methods: The chondrocytes were obtained from the human cartilage tissues. Cells were stimulated by TBHP and treated with hydrogen. In vitro treatment effects were evaluated by Western blot assay, real-time PCR, immunofluorescence and TUNEL method. We conducted mice model of destabilization of the medial meniscus (DMM) and treated with hydrogen. In vivo treatment effects were evaluated by X-ray imaging assay, safranin O (SO) staining, TUNEL staining and immunohistochemical assay. Results: Our results showed that hydrogen can inhibit inflammatory factors (ADAMTS5 and MMP13) and apoptosis factors (cleaved caspase-3, cytochrome c, and Bax) in TBHP-induced chondrocytes. Furthermore, hydrogen can suppress the activation of JNK signaling pathway, whereas the effect of hydrogen can be abolished by anisomycin (a JNK activator). In vivo results showed that hydrogen can down-regulate the expression of p-JNK and cleaved caspase-3 expression. Conclusion: We uncovered that hydrogen (H2) could alleviate apoptosis response and ECM degradation in human chondrocytes via inhibiting the activation of the JNK signaling pathway. Meanwhile, in the surgically-induced DMM mice model, treatment with hydrogen (H2) performed a significant role in OA progression.