中文摘要：

目的探讨硫化氢／胱硫醚-γ-裂解酶（H2S／CSE）体系在内毒素所致大鼠急性肺损伤（ALI）中的作用并初探其机制。方法将64只SD大鼠随机分为对照组、ALI组[经气管内滴注脂多糖（LPS）复制ALI模型]、硫氢化钠（NaHS）组和炔丙基甘氨酸（PPG）组，各组再分为给药后4h和8h亚组，每个亚组8只。于各时间点处死动物，光镜下观察肺组织病理学改变；化学法检测血浆H2S、一氧化氮（NO）和一氧化碳（CO）含量、肺组织丙二醛（MDA）含量、髓过氧化物酶（MPO）、CSE、诱生型一氧化氮合酶（iNOS）和血红素加氧酶（HO）活性；放射免疫法检测肺组织P-选择素含量，用免疫组化法检测肺组织iNOS、HO-1的蛋白表达。结果气管内滴注LPS可引起肺组织明显的病理学改变；肺组织MDA含量、MPO活性和P-选择素水平升高，血浆iNOS、HO活性和肺组织iNOS、HO-1蛋白表达增强，血浆NO、CO含量增加，血浆H2S含量和肺组织CSE活性下降（P〈0．05或P〈0．01）。预先给予NaHS可显著减轻内毒素所致上述指标的改变；而预先给予PPG可加重内毒素所致肺损伤。使肺组织MDA含量、MPO活性、P-选择素水平，血浆NO含量，肺组织iNOS活性和iNOS蛋白表达进一步增加，但对血浆CO含量、肺组织HO活性和HO-1蛋白表达无明显影响。结论H2S／CSE体系的下调在内毒素所致大鼠ALI的发病学中有一定作用，内、外源性H2S具有抗内毒素所致ALI的作用，该作用可能与其抗氧化效应、减轻中性粒细胞所致肺过度的炎症反应以及下调N0／iNOS体系、上调CO／HO-1体系有一定关系。

英文摘要：

Objective To explore the role of hydrogen sulfide/cystathionine-γ-lyase （H2S/CSE） system in lipopolysaecharide （LPS）-induced acute lung injury （ALI） in rats and the underlying mechanisms. Methods Sixty-four Sprague-Dawley （SD） rats were randomly divided into four groups： control, LPS （instilled intratracheally to induce ALI）, sodium hydrosulfide （NariS）, propargylglycin （PPG）. Animals were sacrificed at 4 and 8 hours （n = 8） after administration of the above agents. Morphological changes in lung tissues were determined, H2S, nitrogen monoxide （NO） and carbon monoxide （CO） concentration in plasma were determined. Malondialdehyde （MDA） content, and myeloperoxidase （MPO）, CSE, inducible nitric oxide synthase （iNOS）, hemeoxygenase （HO） activity of the lung were also determined. The level of P-selectin of lung tissue was measured by radioimmunoassay. Immunohistochemisty technique was performed to examine the expression of iNOS and HO-1 protein in lung tissues. Results Severe injuries of lung tissues and raised MDA content, MPO activity and P-seleetin level were observed in rats treated with LPS. LPS also led to a drop in plasma H2S concentration and lung CSE activity. The enzyme activity of iNOS and HO, and their protein expression, plasma NO, and CO levels increased after LPS instillation （P〈0. 05 or P〈0.01）. Pre-administration of Naris before LPS could attenuate the changes induced by LPS. Pre-administration of PPG exacerbated the injuries induced by LPS, with increased MDA content, MPO activity, P-selectin level, the plasma NO level, lung iNOS activity and its protein expression, but there was no prominent variation in CO level, HO activity and HO-1 protein expression compared with those of LPS group. Conclusion Downregulation of H2S/CSE is involved in the pathogenesis of ALI induced by LPS. Endogenous and exogenous H2S provide protection against ALI, which may be explained by its anti-oxidative effects, attenuation of inflammatory over-reaction in