(-)-Epigallocatechin-3-gallate Reduces Cigarette Smoke-Induced Airway Neutrophilic Inflammation and Mucin Hypersecretion in Rats.
(-)-Epigallocatechin-3-gallate Reduces Cigarette Smoke-Induced Airway Neutrophilic Inflammation and Mucin Hypersecretion in Rats.
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DOI：
10.3389/fphar.2017.00618
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发表时间：
2017
影响因子：
5.6
通讯作者：
Mak JCW
中科院分区：
文献类型：
--
作者：
Liang Y;Liu KWK;Yeung SC;Li X;Ip MSM;Mak JCW
背景：吸烟是慢性阻塞性肺疾病的主要原因。表没食子儿茶素没食子酸酯(EGCG)是中国绿茶中的主要儿茶素，已在细胞和动物模型中研究了其抗氧化和抗炎特性。在本研究中，我们旨在分析EGCG对香烟烟雾(CS)诱导的大鼠呼吸道炎症和粘液分泌的影响。方法：雄性SD大鼠随机分为假空气(SA)组和CS组。EGCG(50 mg/kg b.wt.)在SA和CS暴露的动物中每隔一天口服一次。血清和/或支气管肺泡灌洗液中氧化应激和炎症标志物的测定采用生化分析或酶联免疫吸附试验。用高碘酸-席夫染色、Masson‘s三色染色和免疫组织化学方法观察肺组织的形态变化。Western印迹分析探讨EGCG对表皮生长因子受体(EGFR)介导的信号通路的影响。结果：(-)-表没食子儿茶素没食子酸酯处理可减轻CS诱导的氧化应激、肺细胞因子诱导的中性粒细胞趋化因子-1释放和中性粒细胞募集。CS暴露可引起杯状细胞数量增加，与MUC5AC表达上调一致，并增加肺组织胶原沉积，而EGCG可减轻这一作用。此外，EGCG可抑制CS诱导的大鼠肺组织中EGFR的磷酸化。结论：表没食子儿茶素没食子酸酯治疗可减轻CS诱导的大鼠氧化应激和中性粒细胞炎症，减轻气道黏液生成和胶原沉积。提示EGCG对慢性气道炎和气道粘液异常产生有治疗作用，其作用机制可能与抑制EGFR信号通路有关。
Background: Cigarette smoking is the leading cause of chronic obstructive pulmonary disease. (-)-Epigallocatechin-3-gallate (EGCG), the major catechins in Chinese green tea, has been studied for its anti-oxidative and anti-inflammatory properties in cell and animal models. In this study, we aimed to analyze the effects of EGCG on cigarette smoke (CS)-induced airway inflammation and mucus secretion in the CS-exposed rat model. Methods: Male Sprague-Dawley rats were randomly divided into either sham air (SA) or CS exposure. EGCG (50 mg/kg b.wt.) was given by oral gavage every other day in both SA and CS-exposed animals. Oxidative stress and inflammatory markers were determined in serum and/or bronchoalveolar lavage fluid by biochemical assays or ELISA. Lung morphological changes were examined by Periodic Acid-Schiff, Masson’s Trichrome staining and immunohistochemical analysis. Western blot analysis was performed to explore the effects of EGCG on epidermal growth factor receptor (EGFR)-mediated signaling pathway. Results: (-)-Epigallocatechin-3-gallate treatment attenuated CS-induced oxidative stress, lung cytokine-induced neutrophil chemoattractant-1 release and neutrophil recruitment. CS exposure caused an increase in the number of goblet cells in line with MUC5AC upregulation, and increased lung collagen deposition, which were alleviated in the presence of EGCG. In addition, CS-induced phosphorylation of EGFR in rat lung was abrogated by EGCG treatment. Conclusion: (-)-Epigallocatechin-3-gallate treatment ameliorated CS-induced oxidative stress and neutrophilic inflammation, as well as airway mucus production and collagen deposition in rats. The present findings suggest that EGCG has a therapeutic effect on chronic airway inflammation and abnormal airway mucus production probably via inhibition of EGFR signaling pathway.
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影响因子：
5.3
作者：
Li X;Zhang Y;Liang Y;Cui Y;Yeung SC;Ip MS;Tse HF;Lian Q;Mak JC
通讯作者：
Mak JC