Department of Emergency, The Military General Hospital of Beijing PLA, Beijing 100700, China.
Osteoporos Int. 2013 Mar;24(3):969-78. doi: 10.1007/s00198-012-2028-4. Epub 2012 May 31.
Treatment with molecular hydrogen alleviates microgravity-induced bone loss through abating oxidative stress, restoring osteoblastic differentiation, and suppressing osteoclast differentiation and osteoclastogenesis.
Recently, it has been suggested that hydrogen gas exerts a therapeutic antioxidant activity by selectively reducing cytotoxic reactive oxygen species (ROS). The aim of the present study was to elucidate whether treatment with molecular hydrogen alleviated bone loss induced by modeled microgravity in rats.
Hindlimb suspension (HLS) and rotary wall vessel bioreactor were used to model microgravity in vivo and in vitro, respectively. Sprague-Dawley rats were exposed to HLS for 6 weeks to induced bone loss and simultaneously administrated with hydrogen water (HW). Then, we investigated the effects of incubation with hydrogen-rich medium (HRM) on MC3T3-E1 and RAW264.7 cells exposed to modeled microgravity.
Treatment with HW alleviated HLS-induced reduction of bone mineral density, ultimate load, stiffness, and energy in femur and lumbar vertebra. Treatment with HW alleviated HLS-induced augmentation of malondialdehyde content and peroxynitrite content and reduction of total sulfhydryl content in femur and lumbar vertebra. In cultured MC3T3-E1 cells, incubation with HRM inhibited modeled microgravity-induced ROS formation, reduction of osteoblastic differentiation, increase of ratio of receptor activator of nuclear factor kappa B ligand to osteoprotegerin, inducible nitric oxide synthetase upregulation, and Erk1/2 phosphorylation. In cultured RAW264.7, incubation with HRM aggravated modeled microgravity-induced ROS formation, osteoclastic differentiation, and osteoclastogenesis.
Treatment with molecular hydrogen alleviates microgravity-induced bone loss in rats. Molecular hydrogen could thus be envisaged as a nutritional countermeasure for spaceflight but remains to be tested in humans.
通过减轻氧化应激、恢复成骨细胞分化、抑制破骨细胞分化和破骨细胞形成，分子氢治疗可缓解微重力引起的骨丢失。
最近，有研究表明氢气通过选择性地减少细胞毒性活性氧（ROS）发挥治疗性抗氧化作用。本研究旨在阐明分子氢治疗是否可缓解大鼠模拟微重力引起的骨丢失。
采用后肢悬吊（HLS）和旋转壁式生物反应器分别在体内和体外模拟微重力。将 Sprague-Dawley 大鼠暴露于 HLS 中 6 周以诱导骨丢失，并同时给予富氢水（HW）。然后，我们研究了在暴露于模拟微重力的 MC3T3-E1 和 RAW264.7 细胞中孵育富含氢气的培养基（HRM）对细胞的影响。
HW 治疗可减轻 HLS 引起的股骨和腰椎骨矿物质密度、最大载荷、刚度和能量降低。HW 治疗可减轻 HLS 引起的股骨和腰椎丙二醛含量和过氧亚硝酸盐含量增加以及总巯基含量降低。在培养的 MC3T3-E1 细胞中，孵育 HRM 可抑制模拟微重力引起的 ROS 形成、成骨细胞分化减少、核因子κB 配体受体/骨保护素比值增加、诱导型一氧化氮合酶上调和 Erk1/2 磷酸化。在培养的 RAW264.7 细胞中，孵育 HRM 可加重模拟微重力引起的 ROS 形成、破骨细胞分化和破骨细胞形成。
分子氢治疗可缓解大鼠微重力引起的骨丢失。因此，分子氢可以被设想为一种针对太空飞行的营养对策，但仍需在人体中进行测试。
