来自东华大学和第二军医大学药学院的关于氢气对自发性高血压大鼠效应的研究，最近被Biochemical Pharmacology（4.9）接受并在线发表。

    这个研究虽然在研究套路上没有什么新意，但应该是关于高血压的第一篇研究，这里作为常规记录。（近闻美国p大的Nakao教授准备中断氢气的研究，他是临床医生，觉得氢气的研究涉及太多利益冲突，也就是说许多从事氢气商业的公司可能对氢气的研究有太多的影响。Nakao教授 在氢气和器官移植方面有许多开创性的研究，如果他退出这个领域，将是氢气生物学研究的巨大损失。由此想到，许多涉及到利益的研究对学术可能有正面促进作用，也有可能使学术被利益绑架，导致学者失去客观描述研究成果底线。）

    高血压患者氧化应激是导致血管功能异常的重要因素。最近研究表明，氢气作为一种抗氧化物质可以选择性中和强毒性自由基（羟基自由基和亚硝酸阴离子）。本研究观察用氢气生理盐水慢性给药对高血压后血管功能异常的治疗作用及其机制。8周年龄自发高血压大鼠和对照Wistar-Kyoto 鼠随机分为氢气盐水治疗组（6 mg/kg/d3月腹腔注射）对照组。氢气盐水治疗组可显著改善异常的血管功能，包括血管增生和内皮细胞异常。氢气治疗对血压无明显影响，但可以显著提高压力感受反射功能。特别对高血压后氧化应激具有显著的改善作用，包括抗氧化酶（SODCATGpxNADP氧化酶等），对炎症反应如炎症因子和相关信号分子也有显著影响。对线粒体功能也有正面作用，虽然对一氧化氮的产物没有影响，但可以抑制eNOS的表达，促进二甲基精氨酸二甲胺水解酶(DDAH)表达，说明对内皮细胞功能有改善作用。

Chronic hydrogen-rich saline treatment attenuates vascular dysfunction in spontaneous hypertensive rats

·         Hao Zheng^{a, 1}, Yong-Sheng Yu^{b, 1, ,}

·         ^a Department of Pharmaceutical Science and Technology, College of Chemistry and Biology, Donghua University, Shanghai, China

·         ^b Department of Pharmacology, Second Military Medical University, Shanghai, China

·         Received 13 November 2011. Revised 24 January 2012. Accepted 27 January 2012. Available online 8 February 2012.

·         http://dx.doi.org/10.1016/j.bcp.2012.01.031, How to Cite or Link Using DOI

Abstract

。The 8-week-old spontaneously hypertensive rats (SHR) and age-matched Wist ar-Kyoto rats (WKY) were randomized into HRS-treated (6 ml/k

In hypertensive patients, increased oxidative stress is thought to be one important cause of vascular dysfunction. Recently, it has been suggested that hydrogen exerts a therapeutic antioxidant activity by selectively reducing hydroxyl radical and peroxynitrite, the most cytotoxic chemicals of reactive oxygen species (ROS). Herein, we investigated the protective effect of chronic treatment with hydrogen-rich saline (HRS) against vascular dysfunction in SHR and the underlying mechanism.

g/d for 3 months, i.p.) and vehicle treated group. Treatment with HRS ameliorated vascular dysfunction including aortic hypertrophy and endothelial function in SHR.

Treatment with HRS had no significant effect on blood pressure, but it signi ntly improved baroreflex function in SHR. Treatment with HRS abated oxidative stress, restored antioxidant enzymes including superoxide dismutase, glutathione peroxidase, and catalase, and suppressed NADPH oxidase. Furthermore, treatment with HRS depressed pro-inflammatory cytokines expression including IL-6 and IL-1β and suppressed NF-κB activation, restored mitochondrial function including ATP formation and membrane integrity. In addition, although treatment with HRS had no significant effect on nitric oxide amount in circulating or aorta, it suppressed endothelial nitric oxide synthase expression and upregulated dimethylarginine dimethylaminohydrolase 2 expression in SHR. In conclusion, treatment with HRS alleviates vascular dysfunction through abating oxidative stress, restoring baroreflex function, suppressing inflammation, preserving mitochondrial function, and enhancing nitric oxide bioavailability.