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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。
In this paper, acute lung injury (ALI) model of Sprague-Dawley rats and polymorphonuclear neutrophil (PMN) were induced by lipopolysaccharide (LPS) injection in the tail vein. Effect of hydrogen sulfide (H2S) donor sodium hydrosulfide (NaHS) on PMN accumulation, microvessel permeability and PMN apoptosis induced by LPS in lung. Whole experiment and in vitro experiment were set up control group, NaHS group, LPS group and LPS + NaHS group, respectively. Pulmonary microvascular permeability, PMN accumulation in lung and PMN apoptosis were detected. The results showed that: (1) In the whole experiment, the content of protein, the number of PMN and the content of Evans blue in bronchoalveolar lavage fluid (BALF) were significantly higher in LPS group (P <0.05). The above indexes in LPS + NaHS group were significantly lower than those in LPS group (P <0.05, P <0.01). (2) The apoptosis of PMN in human blood PMN, LPS and NaHS groups The percentage was significantly higher than that of the control group (P <0.01), and the LPS + NaHS group was significantly higher than the LPS group (P <0.01). The above results suggest that NaHS can reduce the PMN accumulation in the lungs to a certain extent, play an anti-LPS-induced pulmonary microvascular hyperlipidemia characterized by the role of ALI, promote PMN apoptosis may be the reduction of PMN in the lungs One of the mechanisms of aggregation.