Department of Pediatric Pulmonology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Department of Orthopedics, Shengjing Hospital of China Medical University, Shenyang North New Area, Shenyang, Liaoning 110122, P.R. China.
Mol Med Rep. 2018 Aug;18(2):2088-2096. doi: 10.3892/mmr.2018.9183. Epub 2018 Jun 18.
The present study aimed to investigate the effect of epigallocatechin gallate (EGCG) on airway inflammation in mice with bronchial asthma, and the regulatory mechanism of transforming growth factor (TGF)‑β1 signaling pathway, so as to provide theoretical basis for research and development of a novel drug for clinical treatment. Mouse models of bronchial asthma were established and injected with dexamethasone and EGCG via the caudal vein. 7 days later, bronchoalveolar tissue was collected for hematoxylin and eosin staining. Determination of airway resistance (AWR) and lung function in mice was detected. Serum was separated for cytometric bead array to detect the changes in inflammatory factors. Bronchoalveolar lavage fluid was collected for eosinophil and neutrophil counts. Fresh blood was obtained for flow cytometry to determine the percentages of Th17 and Treg cells. Bronchovesicular tissue was utilized for western blot assay and reverse transcription‑quantitative polymerase chain reaction to determine the proteins and transcription factors in the TGF‑β1 pathway. EGCG 20 mg/kg significantly reduced asthmatic symptoms, lung inflammatory cell infiltration, and the inflammatory factor levels of interleukin (IL)‑2, IL‑6 and tumor necrosis factor (TNF)‑α. In addition, it increased the levels of inflammatory factors, including IL‑10, diminished the percentage of Th17 cells, increased the percentage of Treg cells, and decreased the expression of TGF‑β1 and phosphorylated (p)‑Smad2/3 expression. Following the inhibition of the TGF‑β1 receptor, the anti‑inflammatory effect of EGCG disappeared, and the expression of TGF‑β1 and p‑Smad2/3 increased. EGCG attenuated airway inflammation in asthmatic mice, decreased the percentage of Th17 cells and increased the percentage of Treg cells. The anti‑inflammatory effect of EGCG is achieved via the TGF‑β1 signaling pathway.
本研究旨在探讨表没食子儿茶素没食子酸酯（EGCG）对支气管哮喘小鼠气道炎症的影响及其转化生长因子（TGF）-β1 信号通路的调节机制，为临床治疗新药的研发提供理论依据。通过尾静脉注射地塞米松和 EGCG 建立支气管哮喘小鼠模型。7 天后，收集支气管肺泡组织进行苏木精和伊红染色。检测小鼠气道阻力（AWR）和肺功能。分离血清，通过流式细胞术检测炎症因子的变化。收集支气管肺泡灌洗液，用于嗜酸性粒细胞和中性粒细胞计数。采集新鲜血液，通过流式细胞术测定 Th17 和 Treg 细胞的百分比。利用支气管肺泡组织进行 Western blot 检测和逆转录-定量聚合酶链反应，测定 TGF-β1 通路中的蛋白和转录因子。EGCG 20mg/kg 可显著减轻哮喘症状、肺炎症细胞浸润及白细胞介素（IL）-2、IL-6 和肿瘤坏死因子（TNF）-α等炎症因子水平。此外，还可增加 IL-10 等炎症因子水平，降低 Th17 细胞百分比，增加 Treg 细胞百分比，降低 TGF-β1 和磷酸化（p）-Smad2/3 表达。抑制 TGF-β1 受体后，EGCG 的抗炎作用消失，TGF-β1 和 p-Smad2/3 的表达增加。EGCG 可减轻哮喘小鼠气道炎症，降低 Th17 细胞百分比，增加 Treg 细胞百分比。EGCG 通过 TGF-β1 信号通路发挥抗炎作用。
