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首页> 外文期刊>Journal of Cellular Physiology >Tannic acid attenuates TGF‐β1‐induced epithelial‐to‐mesenchymal transition by effectively intervening TGF‐β signaling in lung epithelial cells
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Tannic acid attenuates TGF‐β1‐induced epithelial‐to‐mesenchymal transition by effectively intervening TGF‐β signaling in lung epithelial cells

机译：丹宁酸变弱TGFβ1应承担的诱导上皮~列车间充质转变有效地干预TGFβ信号在肺上皮细胞

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摘要

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and an irreversible lung disorder characterized by the accumulation of fibroblasts and myofibroblasts in the extracellular matrix. The transforming growth factor‐β1 (TGF‐β1)‐induced epithelial‐to‐mesenchymal transition (EMT) is thought to be one of the possible sources for a substantial increase in the number of fibroblasts/myofibroblasts in IPF lungs. Tannic acid (TA), a natural dietary polyphenolic compound has been shown to possess diverse pharmacological effects. However, whether TA can inhibit TGF‐β1‐mediated EMT in lung epithelial cells remains enigmatic. Both the human adenocarcinomic alveolar epithelial (A549) and normal bronchial epithelial (BEAS‐2B) cells were treated with TGF‐β1 with or without TA. Results showed that TA addition, markedly inhibited TGF‐β1‐induced EMT as assessed by reduced expression of N‐cadherin, type‐1‐collagen, fibronectin, and vimentin. Furthermore, TA inhibited TGF‐β1‐induced cell proliferation through inducing cell cycle arrest at G0/G1 phase. TGF‐β1‐induced increase in the phosphorylation of Smad (Smad2 and 3), Akt as well as that of mitogen activated protein kinase (ERK1/2, JNK1/2, and p38) mediators was effectively inhibited by TA. On the other hand, TA reduced the TGF‐β1‐induced increase in TGF‐β receptors expression. Using molecular docking approach, FTIR, HPLC and Western blot analyses, we further identified the direct binding of TA to TGF‐β1. Finally, we conclude that TA might directly interact with TGF‐β1, thereby repressing TGF‐β signaling and subsequent EMT process in lung epithelial cells. Further animal studies are needed to clarify its potential therapeutic benefit in pulmonary fibrosis.
机译：特发性肺纤维化(IPF)是一种慢性,进步和不可逆肺疾病以成纤维细胞的积累并在细胞外基质myofibroblasts。转化生长因子β1地理地理(TGFβ1)诱导上皮~间充质过渡(EMT)被认为是其中一个大幅增加的可能来源成纤维细胞/ myofibroblasts IPF的数量肺。多酚化合物已被证明不同的药理作用。助教还可以抑制TGFβ1介导EMT在肺上皮细胞仍是神秘的。人类adenocarcinomic肺泡上皮(A549)和正常支气管上皮细胞(比阿斯还是2 b)服用TGFβ1与或没有助教。结果表明,助教,明显抑制TGFβ1应承担的诱导EMT的评估减少N高钙粘蛋白的表达地理地理类型1胶原、纤连蛋白和波形蛋白。此外,TA抑制TGFβ1应承担的诱导细胞通过诱导细胞周期阻滞扩散在G0 / G1期。的磷酸化Smad (Smad2和3),一种蛋白激酶有丝分裂原激活的蛋白激酶(ERK1/2 JNK1/2和p38)介质有效地抑制了助教。TA减少了TGFβ1应承担的必经诱导增加TGFβ受体的表达。方法,红外光谱、高效液相色谱法和免疫印迹分析我们进一步确认助教的直接绑定转化生长因子β1。直接与TGFβ1应承担的交互,从而抑制TGFβ信号和随后的EMT过程肺上皮细胞。需要澄清其潜在的治疗在肺纤维化中获益。

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