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 influence of sulfur dioxide (SO2) on lipopolysaccharide (LPS)-induced acute lung injury (ALI), we examined the influence of exogenous SO2 on pulmonary tissue inflammatory response. A rat model of ALl induced by intravenous (IV) injection of LPS was developed. Male Sprague-Dawley (SD) rats were divided into four groups randomly: control group, LPS group, LPS plus SO2 group (IV injection of 0.5 mL Na2SO3/NaHSO3 10 min before LPS administration) and SO2 group (only given NaESO3/NaHSO3). Animals were sacrificed 6 h after agent administration. Lung weight/body weight ratio (LW/BW) was measured and calculated. Morphological changes of lung tissues were observed. The number of polymorphonuclear neutrophil (PMN) in the bronchoalveolar lavage fluid (BALF), intercellular adhesion factor-1 (ICAM-1) expression in the lung tissue and IL-1, IL-6 and IL-10 levels in the serum were tested. The results showed that, compared to control rats, the LPS-treated rats had severe injuries of lung tissues and an increased LW/BW, increased index of quantitative assessment (IQA) score, increased PMN number in the BALF, increased ICAM-1 expression in the lung tissue and increased IL-1, IL-6 and IL-10 levels in the serum 6 h after LPS injection. Administration of the SO2 donor, Na2SO3/NaHSO3, into LPS-treated rats reduced the LW/BW, PMN number and ICAM-1 expression, and alleviated the degree of ALI (measured by the IQA score). In addition, Na2SO3/NaHSO3 decreased IL-1 and IL-6 levels, but increased IL-10 level in the serum. There were no significant differences in the above indexes between SO2-treated rats and control rats. These results suggest that exogenous SO2 could inhibit the pulmonary tissue inflammatory response in rats with LPS-induced ALI.