Hydrogen Therapy Protects Bone Cells From Inflammatory Damage
- Authors
- Wen-Wen Cai, Ming-Hua Zhang, Yong-Sheng Yu, Jin-Hua Cai
- Journal
- Molecular and Cellular Biochemistry
- Year
- 2013
- DOI
- 10.1007/s11010-012-1450-4
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Rheumatoid Arthritis
- Body System
- Musculoskeletal
TL;DR
Breathing in hydrogen gas can protect bone cells from damage caused by inflammation.
Key Finding
Hydrogen gas reversed TNFα-induced damage to bone-forming cells by reducing oxidative stress, restoring mitochondrial function, and suppressing inflammatory signaling pathways.
Summary
Researchers studied whether hydrogen gas could protect bone-forming cells (osteoblasts) from damage caused by TNFα, a protein involved in inflammatory diseases like rheumatoid arthritis. Using rat bone cells grown in a lab, they found that hydrogen gas reversed the harmful effects of TNFα by reducing oxidative stress (cellular damage from unstable molecules), restoring energy production in cells, and reducing inflammation.
Practical Takeaway
This laboratory study in isolated rat cells suggests hydrogen may have anti-inflammatory and antioxidant effects relevant to bone health, but it is far too early to draw conclusions about benefits in humans. Animal and cell studies often do not translate to human effects, and human trials would be needed to determine if hydrogen water has any actual therapeutic value for bone diseases.
Abstract
Tumor necrosis factor-alpha (TNFα) plays a crucial role in inflammatory diseases such as rheumatoid arthritis and postmenopausal osteoporosis. Recently, it has been demonstrated that hydrogen gas, known as a novel antioxidant, can exert therapeutic anti-inflammatory effect in many diseases. In this study, we investigated the effect of treatment with hydrogen molecule (H2) on TNFα-induced cell injury in osteoblast. The osteoblasts isolated from neonatal rat calvariae were cultured. It was found that TNFα suppressed cell viability, induced cell apoptosis, suppressed Runx2 mRNA expression, and inhibited alkaline phosphatase activity, which was reversed by co-incubation with H2. Incubation with TNFα-enhanced intracellular reactive oxygen species (ROS) formation and malondialdehyde production increased NADPH oxidase activity, impaired mitochondrial function marked by increased mitochondrial ROS formation and decreased mitochondrial membrane potential and ATP synthesis, and suppressed activities of antioxidant enzymes including SOD and catalase, which were restored by co-incubation with H2. Treatment with H2 inhibited TNFα-induced activation of NFκB pathway. In addition, treatment with H2 inhibited TNFα-induced nitric oxide (NO) formation through inhibiting iNOS activity. Treatment with H2 inhibited TNFα-induced IL-6 and ICAM-1 mRNA expression. In conclusion, treatment with H2 alleviates TNFα-induced cell injury in osteoblast through abating oxidative stress, preserving mitochondrial function, suppressing inflammation, and enhancing NO bioavailability.