山莨菪碱对急性肺损伤时肺泡巨噬细胞分泌细胞因子的干预探讨

目的观察山莨菪碱(654-2)对急性肺损伤(ALI)大鼠肺泡巨噬细胞(AM)分泌肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)的影响，探讨其对ALI治疗作用的可能机制。方法复制ALI大鼠模型。实验动物随机分为ALI模型组、654-2治疗组、对照组，进行各组大鼠动脉血气、肺湿／干(W／D）值测定及肺组织病理学光镜检查。分离培养各组大鼠肺泡巨噬细胞，采用生物活性法进行AM上清液TNF-α、IL-6测定。结果654-2治疗组大鼠AM分泌TNF-α［（38．98±4.51)KU/L］和IL-6［（20．82±6.3)kU/L］的水平明显低于ALI组［TNF-α为(68.27±9.13)kU/L，P＜0.001；IL-6为(33.84±9.02)kU/L，P＜0.01］，并能使血气改善(P＜0.05)、W／D值下降(P＜0.05)，肺组织损伤程度减轻。结论654-2对ALI大鼠肺泡巨噬细胞过度活化、分泌TNF-α、IL-6具有显著抑制作用，在一定程度上防止ALI的发生和发展。

Studies of Anisodamine in treatment of ALI and its effects on cytokine secretion in alveolar macrophages

Objective　To explore the mechanism of anisodamine(654-2) in the treatment of acute lung injury(ALI),the effect of 654-2 on TNF-α and IL-6 levels released by alveolar macrophages were investigated in rats.Methods　ALI rats model was made by injection of lipopolysaccharide(LPS) intravenously.48 rats were equally divided into three groups:ALI model group,654-2 treatment group and normal control group.The bloods air,lung wet/dry (W/D) weight and pathological examination were made in each groups.Then the alveolar macrophages of each group were separated and cultured,the quantities of TNF-α and IL-6 were measured by bioassa methods.Results　TNF-α　［(38.98±4.51)kU/L］ and IL-6［(20.82±6.3)kU/L］levels released by alveolar macrophages in 654-2 treatment group were significantly lower than those of ALI group ［TNF-α(68.27±9.13)kU/L,P＜0.001］；IL-6［（33.84±9.02)kU/L,P＜0.01］and 654-2 can also improve the blood airs levels(P＜0.05),reduce the W/D value (P＜0.05) and relieve the lung injury observed by histological examination.Conclusion　654-2 can inhibit the excessive activation and TNF-α,IL-6 secretion of alveolar macrophages,prevent the occurrance progression of ALI in rats.