Molecular Hydrogen Ameliorates Lipopolysaccharide-Induced Acute Lung Injury in M.pdf

来自天津医科大学附属医院谢克亮等的文章最近发表在世界著名杂志《休克》上，文章是关于呼吸氢气对LPS诱导急性肺损伤保护机制的研究。

急性肺损伤是导致临床危重病患者死亡的最重要因素。最近国际上研究证明氢气可以治疗脓毒症、机械通气、高氧和缺血再灌注后肺损伤。但关于上述作用的具体分子机制不明确。在该研究中，作者通过观察呼吸氢气和注射含氢气生理盐水对LPS诱导的肺损伤的作用，结果发现，呼吸氢气和折射氢气盐水都可以显著改善LPS诱导的肺损伤后细胞凋亡和炎症反应。

Molecular Hydrogen Ameliorates Lipopolysaccharide-Induced Acute Lung Injury in Mice Through Reducing Inflammation and Apoptosis. Shock. 2012 May;37(5):548-555.

Abstract

Acute lung injury (ALI) is still a leading cause of morbidity and mortality in critically ill patients. Recently, our and other studies have found that hydrogen gas (H2) treatment can ameliorate the lung injury induced by sepsis, ventilator, hyperoxia, and ischemia-reperfusion. However, the molecular mechanisms by which H2 ameliorates lung injury remain unclear. In the current study, we investigated whether H2 or hydrogen-rich saline (HS) could exert protective effects in a mouse model of ALI induced by intratracheal administration of lipopolysaccharide (LPS) via inhibiting the nuclear factor κB (NF-κB) signaling pathway-mediated inflammation and apoptosis. Two percent of H2 was inhaled for 1 h beginning at 1 and 6 h after LPS administration, respectively. We found that LPS-challenged mice exhibited significant lung injury characterized by the deterioration of histopathology and histologic scores, wet-to-dry weight ratio, and oxygenation index (PaO2/FIO2), as well as total protein in the bronchoalveolar lavage fluid (BALF), which was attenuated by H2 treatment. Hydrogen gas treatment inhibited LPS-induced pulmonary early and late NF-κB activation. Moreover, H2 treatment dramatically prevented the LPS-induced pulmonary cell apoptosis in LPS-challenged mice, as reflected by the decrease in TUNEL (deoxynucleotidyl transferase dUTP nick end labeling) staining-positive cells and caspase 3 activity. Furthermore, H2 treatment markedly attenuated LPS-induced lung neutrophil recruitment and inflammation, as evidenced by downregulation of lung myeloperoxidase activity, total cells, and polymorphonuclear neutrophils in BALF, as well as proinflammatory cytokines (tumor necrosis factor α, interleukin 1β, interleukin 6, and high-mobility group box 1) and chemokines (keratinocyte-derived chemokine, macrophage inflammatory protein [MIP] 1α, MIP-2, and monocyte chemoattractant protein 1) in BALF. In addition, i.p. injection of 10 mL/kg hydrogen-rich saline also significantly attenuated the LPS-induced ALI. Collectively, these results demonstrate that molecular hydrogen treatment ameliorates LPS-induced ALI through reducing lung inflammation and apoptosis, which may be associated with the decreased NF-κB activity. Hydrogen gas may be useful as a novel therapy to treat ALI.

PMID: 22508291 [PubMed - as supplied by publisher]