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呼吸氢气对LPS诱导的肺损伤具有保护作用

已有 2838 次阅读 2011-10-21 01:17 |个人分类:呼吸氢气|系统分类:论文交流|关键词:氢气

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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doi:10.1016/j.intimp.2011.09.007 | How to Cite or Link Using DOI

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Hydrogen inhalation ameliorates lipopolysaccharide-induced acute lung injury in mice

Xiaochen Qiua1, Hengyu Lia1, Hongtai Tanga1, Yichao Jinc, Wuquan Lid,  YuSuna,  PingFenga, Xuejun Sunb, Zhaofan Xiaa

a

Burn Center, Changhai Hospital, Second Military Medical University, Shanghai 200433, China

b

Department of Diving Medicine, Second Military Medical University, Shanghai 200433, China

 

c

Department of Pathology, Kunming Medical College, Kunming 650031, China

d

Burn Center of Yunnan Province, Second Affiliated Hospital of Kunming Medical College, Kunming 650101, China

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

 



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