论文部分内容阅读
为探讨外源性二氧化硫(sulfur dioxide,SO2)对脂多糖(lipopolysaccharide,LPS)所致大鼠肺损伤时肺组织炎性反应的影响,采用经尾静脉注射LPS的方法复制大鼠肺损伤模型,将雄性Sprague-Dawley(SD)大鼠随机分为4组:对照组、LPS组、LPS+SO2组[注射LPS前10min静脉给予外源性SO2供体亚硫酸钠/亚硫酸氢钠(Na2SO3/NaHSO3)0.5mL]和SO2组(单纯给予Na2SO3/NaHSO3)。给药后6h处死大鼠,测定肺系数;光镜下观察肺组织形态学改变;测定支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF)中的中性粒细胞(polymorphonuclear neutrophil,PMN)数量;采用流式细胞术检测肺组织中细胞间黏附因子-1(ICAM-1)的表达情况;应用酶联免疫法(ELISA)检测血清中IL-1、IL-6和IL-10含量。所得结果如下:与对照组比较,静脉注射LPS可引起肺组织明显的形态学改变;肺系数、肺损伤的组织学定量评价指标(IQA)和BALF中PMN数量增加;肺组织中ICAM-1表达增多,血清中IL-1、IL-6和IL-10水平升高。预先给予Na2SO3/NaHSO3可显著减轻LPS所致肺损伤的程度,同时使肺系数、肺IQA和BALF中PMN数量减少;肺组织中ICAM-1表达下降,血清中IL-1、IL-6水平下降而IL-10水平升高。SO2组大鼠上述各项指标与对照组大鼠相比无显著差异。以上结果提示,外源性SO2可抑制LPS所致大鼠肺损伤时肺组织中的炎症反应。
To investigate the effect of sulfur dioxide (SO2) on the inflammatory reaction in lung tissue of rats with lipopolysaccharide (LPS) -induced lung injury, the model of lung injury was established by injecting LPS through tail vein. Male Sprague-Dawley rats were randomly divided into 4 groups: control group, LPS group, LPS + SO2 group (exogenous SO2 donor sodium sulfite / sodium bisulfite (Na2SO3 / NaHSO3) 0.5mL] and SO2 group (Na2SO3 / NaHSO3 only). The rats were sacrificed at 6h after administration and the lung coefficient was measured. The morphological changes of lung tissue were observed under light microscope. The number of polymorphonuclear neutrophil (PMN) in bronchoalveolar lavage fluid (BALF) The expression of intercellular adhesion molecule-1 (ICAM-1) in lung tissue was detected by flow cytometry. The levels of IL-1, IL-6 and IL-10 in serum were detected by enzyme-linked immunosorbent assay (ELISA) The results obtained were as follows: Compared with the control group, intravenous injection of LPS caused significant morphological changes in lung tissue; lung coefficient, histological quantitative evaluation index (IQA) of lung injury and PMN increased in BALF; ICAM-1 expression in lung tissue Increased serum levels of IL-1, IL-6 and IL-10 increased. Pretreatment with Na2SO3 / NaHSO3 significantly reduced the degree of lung injury induced by LPS, while decreased the lung coefficient, lung IQA and the number of PMN in BALF. The expression of ICAM-1 in lung tissue decreased and the levels of IL-1 and IL-6 in serum decreased While levels of IL-10 are elevated. There was no significant difference between the above indexes in SO2 group and control group. The above results suggest that exogenous SO2 can inhibit the lung inflammation in LPS-induced lung injury.