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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 (EL ISA)法测定干扰素γ(IFNγ)、白介素 4(IL 4)浓度 ;逆转录聚合酶链反应 (RTPCR)法测定 m RNA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 ,IL 4明显升高 (P均 <0 .0 1)。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 IL 4均明显降低 ,但以 IL 4降低更为显著 (P均 <0 .0 1) ;地塞米松组 IFNγ和 IL 4也明显降低 ,但以 IFNγ下降更为显著 (P<0 .0 1) ;正常对照组、急性肺损伤组、雷公藤多甙组和地塞米松组的 IFNγm RNA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 .0 5 )。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 the changes of T helper lymphocyte (TH, TH1/TH2) in mice with acute lung injury and the effects of tripterygium wilfordii on it. METHODS: Rats with acute lung injury were induced by intraperitoneal injection of lipopolysaccharide and randomly divided into acute lung injury group, tripterygium wilfordii group, dexamethasone group and normal control group (n=8). The concentration of interferon gamma (IFN gamma) and interleukin 4 (IL 4) was determined by enzyme-linked immunosorbent assay (EL ISA), and m RNA expression was measured by reverse transcription polymerase chain reaction (RTPCR). Evans Blue Fluorescence Assay for Determination of Pulmonary Vascular Protein Exudation RESULTS :Compared with the normal control group, IFN-γ in the culture supernatant of splenic lymphocytes in mice with acute lung injury was significantly decreased, and IL 4 was significantly increased (P<0.01). Compared with acute lung injury group: IFNγ and IL 4 were significantly decreased in spleen lymphocyte culture supernatants of mice in the Tripterygium wilfordii group, but the decrease in IL 4 was more significant (P <0.01); dexamethasone. The levels of IFNγ and IL 4 were also significantly decreased, but the decrease of IFNγ was even more significant (P<0.01). The expression of IFNγ mRNA decreased in the normal control group, acute lung injury group, tripterygium wilfordii group and dexamethasone group. . Compared with the acute lung injury group, Evans blue exudation, lung wet/dry weight ratio and polymorphonuclear granulocyte counts in the lung tissue of the Tripterygium wilfordii group and dexamethasone group were significantly reduced (P<0. 0 5 ). Conclusion: Acute lung injury causes TH1 to shift to TH2. Tripterygium glycosides and dexamethasone can prevent and treat acute lung injury by regulating inflammatory responses.