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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。
Objective To observe the effect of epigallocatechin gallate (EGCG) on bleomycin-induced pulmonary fibrosis in rats and its mechanism. Methods Healthy Sprague-Dawley rats were randomly divided into normal group, model group, prednisone group and EGCG large, medium and small dose groups, intratracheal instillation of bleomycin-induced pulmonary fibrosis model, in the second day after modeling After 28 d administration, the lung tissue was taken for histopathological observation and the content of hydroxyproline was determined. The expression of TGF-β1, Smad2 and Smad7 mRNA in lung tissue was detected by RT-PCR expression. Results The pulmonary alveolitis and pulmonary fibrosis of rats in EGCG treatment group were significantly relieved (P <0.05 or <0.01), hydroxyproline content was significantly decreased (P <0.05 or <0.01). The results of RT-PCR showed that the expression of TGF-β1 and Smad2 in EGCG-treated group was down-regulated (P <0.05 or <0.01), and the expression of Smad7 was significantly up-regulated (P <0.05 or <0.01). Conclusion EGCG can reduce bleomycin-induced pulmonary fibrosis in rats, and its mechanism may be related to its regulation of TGF-β1 / Smad signaling pathway.