关于氢气治疗疾病的报道已经很多，似乎对所有氧化应激相关疾病都有治疗作用。从治疗机制上，也基本上是从提高抗氧化酶，减少自由基产生，抑制炎症反应，减少细胞损伤这个角度。但从逻辑上，减少氧化应激和促进细胞抗氧化酶活性往往是矛盾的。目前的解释是氢气不影响具有信号作用的自由基，实质上是在保持氧化应激正面效应的基础上，减少氧化应激的伤害性后果。对炎症的作用也可以用同样的思路来解释。不过，现在的证据仍不全面。

高血压动物和人类，氧化应激是左心室肥大的基础原因。最近研究发现氢气是一种新型抗氧化物质，可以选择性中和毒性自由基，对许多氧化应激性疾病具有很好的治疗效果。本研究观察慢性氢气治疗对高血压后左心室肥大的治疗作用。

8周龄雄性自发性高血压大老鼠，年龄匹配的Wistar-Kyoto为对照，随机分成氢气治疗组，对照治疗组，氢气治疗组给每天每次腹腔注射6 ml/kg，连续3月。结果发现氢气治疗对血压无明显影响（对应文章已经发表该结果），但对左心肥大具有治疗效果。同时氢气治疗可以降低左心室氧化应激，提高抗氧化酶GPx, GST, catalase和SOD等活性,抑制NADPH氧化酶火星，下调Nox2 和Nox4的表达。另外氢气对炎症因子IL-1β, IL-6, TNF-α和 MCP-1有抑制作用，并可以通过IκBα降低NF-κB活性。

氢气治疗还可以通过维持呼吸链酶活性保护线粒体功能，抑制活性氧生成，提高ATP产生能力。氢气对ACE酶的表达也具有抑制作用（果真如此，如果血管中的该酶也有影响的话，为什么不能降低血压），从而可以降低血管紧张素II的产生。

总之，研究结果表明，氢气治疗可以降低高血压引起的左心室肥大。该效应是通过降低氧化应激，抑制炎症反应，保护线粒体功能，而且通过减少ACE酶表达减少管紧张素II的产生。

Mol Cell Biochem. 2012 Feb 18. [Epub ahead of print]

Chronic hydrogen-rich saline treatment reduces oxidative stress and attenuates left ventricular hypertrophy in spontaneous hypertensive rats.

Yu YS, Zheng H.

Source

Department of Pharmacology, College of Pharmacy, Second Military Medical University, Shanghai, 200433, China, yuys1982@hotmail.com.

Abstract

In hypertensive animals and patients, oxidative stress represents the primary risk factor for progression of left ventricular hypertrophy. Recently, it has been demonstrated that hydrogen, as a novel antioxidant, can selectively reduce hydroxyl radicals and peroxynitrite anion to exert therapeutic antioxidant activity. In the current study, we explored the effect of chronic treatment with hydrogen-rich saline (HRS) on left ventricular hypertrophy in spontaneously hypertensive rats (SHR).

The 8-week-old male SHR and age-matched Wistar-Kyoto rats (WKY) were randomized into HRS-treated (6 ml/kg/day for 3 months, i.p.) and vehicle-treated groups. HRS treatment had no significant effect on blood pressure, but it effectively attenuated left ventricular hypertrophy in SHR. HRS treatment abated oxidative stress, restored the activity of antioxidant enzymes including GPx, GST, catalase, and SOD, suppressed NADPH oxidase activity and downregulated Nox2 and Nox4 expression in left ventricles of SHR. HRS treatment suppressed pro-inflammatory cytokines including IL-1β, IL-6, TNF-α, and MCP-1, and inhibited NF-κB activation through preventing IκBα degradation in left ventricles of SHR.

HRS treatment preserved mitochondrial function through restoring electron transport chain enzyme activity, repressing ROS formation, and enhancing ATP production in left ventricles of SHR. Moreover, HRS treatment suppressed ACE expression and locally reduced angiotensin II generation in left ventricles of SHR. In conclusion, HRS treatment attenuates left ventricular hypertrophy through abating oxidative stress, suppressing inflammatory process, preserving mitochondrial function, in which suppression of HRS on angiotensin II in left ventricles locally might be involved.