曾经有研究证明，氢可以缓解失重和卵巢切除情况下动物骨质丢失，主要原因是通过对抗氧化损伤，但关于该效应的分子细节了解不多。本研究在上述研究的基础上，采用细胞学研究方法，着重观察了氢对肿瘤坏死因子诱导的成骨细胞损伤的保护作用，以及相关分子改变。

来自解放军总医院的一项研究，近日发表在Mol Cell Biochem。这是一篇比较典型的描述性细胞学研究。研究的内容相对比较全面，不足的是没有进行纵向和阻断性研究。无法明确这些现象是否属于伴随现象，还是氢作用的主要通路。

肿瘤坏死因子-α（TNFα）在炎症性疾病中起着关键的作用。如类风湿关节炎和绝经后骨质疏松症。最近有证据表明，氢气作为一种新的抗氧化剂，可在许多疾病治疗中发挥抗炎效果。在这项研究中，作者观察了氢分子（H（2）对TNFα-诱导的成骨细胞损伤治疗效果。成骨细胞取自新生鼠颅骨。结果发现，肿瘤坏死因子抑制细胞活力，诱导细胞凋亡，抑制Runx2的mRNA的表达，抑制碱性磷酸酶活性，用H（2）共同孵育可逆转上述改变。肿瘤坏死因子可使细胞内活性氧（ROS）的产生增加、丙二醛含量升高、NADPH氧化酶的活性增加，通过增加线粒体ROS的形成、线粒体膜电位降低和抑制ATP合成，并抑制抗氧化酶活性，包括超氧化物歧化酶和过氧化氢酶，用H（2）共孵育可逆转上述效应。同时H（2）治疗可抑制TNFα诱导的激活的NFκB的途径，抑制TNFα-诱导型一氧化氮（NO）的形成，抑制iNOS活性，抑制TNFα-诱导的IL-6和ICAM-1 mRNA的表达。上述结果提示，H（2）可通过减轻TNFα-诱导的细胞损伤的成骨细胞氧化应激，保护线粒体功能，抑制炎症，提高NO生物利用度。

Mol Cell Biochem. 2012 Dec 1. [Epub ahead of print]

Treatment with hydrogen molecule alleviates TNFα-induced cell injury in

osteoblast.

Cai WW, Zhang MH, Yu YS, Cai JH.

The Centre of Drug Safeguard, Chinese People's Liberation Army General Hospital,

Beijing, People's Republic of China.

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 (H(2)) 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 H(2). 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 H(2). Treatment with H(2) inhibited TNFα-induced activation

of NFκB pathway. In addition, treatment with H(2) inhibited TNFα-induced nitric

oxide (NO) formation through inhibiting iNOS activity. Treatment with H(2)

inhibited TNFα-induced IL-6 and ICAM-1 mRNA expression. In conclusion, treatment

with H(2) alleviates TNFα-induced cell injury in osteoblast through abating

oxidative stress, preserving mitochondrial function, suppressing inflammation,

and enhancing NO bioavailability.

PMID: 23212446  [PubMed - as supplied by publisher]