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呼吸氢气对LPS诱导的肺损伤具有保护作用
作者:admin    发布于:2019-06-14 15:11    文字:【 】【 】【
  LPS诱导的肺损伤具有保护作用
 
全文:Hydrogen inhalation ameliorates lipopolysaccharide-induced acute lung injury in mice.pdf
呼吸氢气对
    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
In Press, Uncorrected Proof - Note to users
doi:10.1016/j.intimp.2011.09.007 | How to Cite or Link Using DOI
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Hydrogeninhalation ameliorates lipopolysaccharide-induced acute lung injury in mice
Xiaochen Qiua, 1, Hengyu Lia, 1, Hongtai Tanga, 1, 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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