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中性粒细胞在外源性硫化氢抗内毒素致急性肺损伤中的作用 被引量:13

Role of polymorphonuclear neutrophil in exogenous hydrogen sulfide attenuating endotoxin-induced acute lung injury
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摘要 本文应用尾静脉注射脂多糖(lipopolysaccharide,LPS)致Sprague-Dawley大鼠急性肺损伤(acute lung injury,ALI)模型和体外培养人血多形核中性粒细胞(polymorphonuclear neutrophil,PMN),观察硫化氢(hydrogen sulfide,H2S)供体硫氢化钠(sodium hydrosulfide,NaHS)对LPS所致肺内PMN聚集、微血管通透性及PMN凋亡的影响。整体实验和体外实验分别设对照组、NaHS组、LPS组和LPS+NaHS组,检测肺微血管通透性、肺内PMN聚集以及PMN凋亡情况。结果显示:(1)整体实验中,LPS组大鼠的支气管肺泡灌洗液(bronchoalveloar lavage fluid,BALF)中蛋白含量、PMN数量、肺组织中伊文思蓝(Evans blue)含量均明显高于假手术组(均P<0.05),而LPS+NaHS组上述指标均明显低于LPS组(P<0.05,P<0.01);(2)体外培养人血PMN,LPS组和NaHS组的PMN凋亡百分率明显高于对照组(P<0.01),LPS+NaHS组明显高于LPS组(P<0.01)。以上结果提示,NaHS能够减少PMN在肺内的聚集,在一定程度上起到抗LPS所致的以肺微血管高通透性为特征的ALI的作用,促进PMN凋亡可能是NaHS减轻PMN在肺内聚集的机制之一。 The animal model of acute lung injury (ALI) caused by intravenous injection of lipopolysaccharides (LPS) and cultured human peripheral blood polymorphonuclear neutrophil (PMN) were used to study the effects of sodium hydrosulfide (NariS), hydrogen sulfide (H2S) donor, on LPS-induced PMN accumulation, microvascular permeability and PMN apoptosis. Control group, NariS group, LPS group and LPS + NariS group were established both in in vivo and in vitro studies. Microvascular permeability, PMN accumulation in lung and apoptosis of PMN were detected. The results showed that: (1) In in vivo study, PMN accumulation in lung, the protein content in bronchoalveolar lavage fluid (BALF) and the Evans blue dye in lung tissue of LPS group were markedly higher than those of both sham operation group and LPS + NariS group (P〈0.05, P〈0.01); (2) In in vitro study, the apoptotic rates of PMN in LPS group and NariS group were significantly higher than that in control group (P〈0.01), while compared with LPS group, LPS + NariS group showed significantly higher apoptotic rate (P〈0.01). These results suggest that NariS attenuates LPS-induced microvascular permeability and alleviates ALI. PMN apoptosis induced by NariS is possibly one of the potential mechanisms underlying the decrease of PMN accumulation in lung tissue.
出处 《生理学报》 CAS CSCD 北大核心 2009年第4期356-360,共5页 Acta Physiologica Sinica
基金 supported by the National Natural Science Foundation of China(No.30800440) the Natural Science Foundation of Hebei Province China(No.C2007000830 C2008001040) the Natural Science Foundation of Beijing Municipality China(No.7092035) the Educational Committee of Hebei Province China(No.2005123)
关键词 硫化氢 内毒素 肺损伤 中性粒细胞 hydrogen sulfide endotoxin acute lung injury polymorphonuclear neutrophil
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