雷公藤多甙对小鼠急性肺损伤的防治作用

摘要

目的：观察急性肺损伤小鼠T 辅助淋巴细胞(TH，TH1/TH2)的变化及雷公藤多甙对其影响。方法：腹腔 注射脂多糖复制小鼠急性肺损伤模型，随机分急性肺损伤组、雷公藤多甙组、地塞米松组和 正常对照组(n=8)。酶联免疫吸附(ELISA)法测定干扰素γ(IFNγ)、白介素4(IL4)浓度;逆转录聚合酶链反应(RTPCR)法测定mRNA表达。伊文思蓝荧光法测定肺血管蛋白渗出量。结果： 与正常对照组比较：急性肺损伤组小鼠脾淋巴细胞培养上清液中IFNγ显著下 降，IL4明显升高(P均<0.01)。与急性肺损伤组比较：雷公藤多甙组小 鼠 脾淋巴细胞培养上清中IFNγ和IL4均明显降低，但以IL4降低更为显著(P均<0.01)；地塞米松组IFNγ和IL4 也 明显降低，但以IFNγ下降更为显著(P<0.01)；正常对照组、急性肺 损伤组、雷公藤多甙组和地塞米松组的IFNγmRNA表达依次下降。与急性肺损 伤组比较：雷公藤多甙组、地塞米松组肺组织中伊文思蓝渗出量、肺湿重/干重比和多形核 粒细胞计数均明显降低(P均<0.05)。结论：急性肺损伤导致TH1 向TH2漂移，雷公藤多甙和地塞米松通过调节炎症反应，对急性肺损伤具有防治作用。%Objective:To observe changes of TH1/TH2 in mice with acute lung injury(ALI)and the influences of tripteryg ium wilfordii(TW，雷公藤多甙) on ALI.Methods:ALI mouse models were established by means of injecting lipopolysaccharide into abdominal cavity then were randomly divided into ALI,TW,dexamethason(DEX),and no rmal control (NC) group. Using enzymelinked immunosorbent assay(ELI SA) method,t he concentrations of interferonγ(IFNγ) and interleukin 4(IL4) were measured and the mRNA expression was detected by reverse transcriptionpolymerase c hain reaction (RTPCR) method,meanwhile the volume of prota in exudation from pulmonary vessels was determined by Evans blue fluorescence m ethod.Results:As c ompared with NC group,IFNγ in supernatant of cultured spleni c lymphocyte was decreased but IL4 was increased(both P<0.01) in ALI group.There was a significant decrease in both IFNγ and IL4 in TW and DEX group in comparison to ALI group.Moreover,IL4 levels in supernatants were signif icant lower in TW group than that in DEX group.On the contrary,IFNγ was significant lower in DEX group than that in TW group.IFNγ mRNA e xpression was decreased in order of NC,ALI,TW and DEX group,successively.A s compared with ALI group,the ratio of lung wet to dry weight, polymorphonuclear leukocyte (PMN) count and the exudation volume of Evans blue were significantly decreased in DEX grou p and TW group(all P<0.05).Conclusions:TH cell may be shift from TH1 to TH2 in ALI.Both TW and DEX can improve ALI by regulating inflammatory response and poss ess preventive and therapeutic effects on ALI.