全文：Hydrogen inhalation ameliorates lipopolysaccharide-induced acute lung injury in mice.pdf

呼吸氢气对LPS诱导的肺损伤具有保护作用

    该研究来自长海医院烧伤科，研究发现呼吸2%的氢气可以提高LPS导致的肺损伤动物存活时间，降低氧化损伤、炎症反应和组织细胞凋亡。结果表明，呼吸氢气对LPS诱导的肺损伤具有保护作用。这是该实验室发表的第4篇关于氢气方面的论文，过去曾经发表小肠缺血保护作用，氢复苏和肝脏损伤保护等方面的论文。本论文提供了一种简易的呼吸氢气的自制装置，有兴趣者可以参考使用，但其中最关键是如何配置混合氢气，这个最好有专业人士操作，建议从气体公司直接购买混合气使用为好。

International Immunopharmacology
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Hydrogen inhalation ameliorates lipopolysaccharide-induced acute lung injury in mice

Xiaochen Qiu^a, 1, Hengyu Li^a, 1, Hongtai Tang^a, 1, Yichao Jin^c, Wuquan Li^d,  YuSun^a,  PingFeng^a, Xuejun Sun^b, Zhaofan Xia^{a,  ,} 

Received 21 June 2011; revised 22 August 2011; Accepted 15 September 2011. Available online 19 October 2011.

Abstract

Acute lung injury (ALI) is a serious illness, the incidence and mortality of which are very high. Free radicals, such as hydroxyl radicals ( OH) and peroxynitrite (ONOO⁻), are considered to be the final causative molecules in the pathogenesis of ALI. Hydrogen, a new antioxidant, can selectively reduce OH and ONOO⁻. In the present study, we investigated the hypothesis that hydrogen inhalation could ameliorate ALI induced by intra-tracheal lipopolysaccharide (LPS, 5 mg/kg body weight). Mice were randomized into three groups: sham group (physiological saline + 2% hydrogen mixed gas ), control group (LPS + normal air) and experiment group (LPS + 2% hydrogen mixed gas ). Bronchoalveolar lavage fluid (BALF) was performed to determine the total protein concentrations and pro-inflammatory cytokines. Lung tissues were assayed for oxidative stress variables, wet/dry (W/D) ratio, histological, immunohistochemistry and Western blotting examinations. Our experiments exhibited that hydrogen improved the survival rate of mice and induced a decrease in lung W/D ratio. In addition, hydrogen decreased malonaldehyde and nitrotyrosine content, inhibited myeloperoxidase and maintained superoxide dismutase activity in lung tissues and associated with a decrease in the expression of TNF-α, IL-1β, IL-6 and total protein concentrations in the BALF. Hydrogen further attenuated histopathological alterations and mitigated lung cell apoptosis. Importantly, hydrogen inhibited the activation of P-JNK, and also reversed changes in Bax, Bcl-xl and caspase-3. In conclusion, our data demonstrated that hydrogen inhalation ameliorated LPS-induced ALI and it may be exerting its protective role by preventing the activation of ROS–JNK–caspase-3 pathway.

Highlights

► Hydrogen inhalation ameliorated the LPS-induced oxidative stress. ► Hydrogen prevented the release of pro-inflammatory molecules and attenuated P-JNK levels. ► Hydrogen inhibited lung cell apoptosis through inhibiting the caspase-3 and Bax and preventing the decrease of Bcl-xl. ► Hydrogen may be exerting its protective role by preventing the activation of ROS–JNK–caspase-3 pathway