表没食子儿茶素没食子酸酯对博莱霉素所致肺纤维化大鼠肺组织中TGF-β1及Smad2/7mRNA表达的影响

目的观察表没食子儿茶素没食子酸酯（EGCG）对博莱霉素所致大鼠肺纤维化的作用及其机制。方法健康SD大鼠随机分为正常组、模型组、泼尼松组及EGCG大、中、小剂量组,经气管内滴注博莱霉素复制肺纤维化模型,于造模后第2天开始给药,给药28 d后,取肺组织作病理形态学观察并测定其羟脯氨酸含量,采用RT-PCR法检测肺组织中转化生长因子（TGF）-β1、Smad2、Smad7 mRNA的表达。结果 EGCG各给药组大鼠肺组织肺泡炎和肺纤维化程度明显减轻（P〈0.05或〈0.01）,羟脯氨酸含量明显降低（P〈0.05或〈0.01）。RT-PCR检测结果显示,EGCG给药组大鼠TGF-β1、Smad2表达下调（P〈0.05或〈0.01）,Smad7表达明显上调（P〈0.05或〈0.01）。结论 EGCG可减轻博莱霉素所致大鼠肺纤维化程度,其作用机制可能与其调控TGF-β1/Smad信号通路有关。

Effect of epigallocatechin gallate（EGCG） on the expression of TGF-β1 and Smad2/7mRNA of lung tissue of the experimental lung pulmonary fibrosis in rats

Objective To investigate the mechanisms of epigalloeatechin gallate （EGCG） on Bleomycin-induce pulmonary fibrosis in rats. Methods Sprague-Dawley rats were randomly divided into control, model, prednisolone group and EGCG large-dose, middle-dose, small-dose group. Pulmonary fibrosis model was established by intratracheal injection of bleomycin （5mg/kg）. Then the rats were treated with corresponding dose of EGCG by intragastric administration. After 28 days, the extent of pulmonary fibrosis was evaluated by histopathological analysis. The extent of pulmonary alveolitis and fibrosis were evaluated by histopathological and biochemical analysis. The level of TGF-β, Smad2 and Smad7 mRNA were assayed by semi-quantitative RT-PCR. Results EGCG reduced the extent of alveolitis, fibrosis （P 〈 0.05 or 〈 0.01 ）, and dramatically decreased the content of HYP in the lung tissue （ P 〈 0.05 or 〈 0.01 ）. EGCG also decreased the level of TGF-β1 ,Smad2 mRNA（P 〈0.05 or 〈0.01 ）while the expression of Smad7 mRNA in lung tissue of rats was significantly increased （P 〈0.05 or 〈 0.01 ）. Conclusion EGCG could alleviated bleomycin-induced pulmonary fibrosis in rats, which might be related with inhibition of TGF-β singnal pathway.