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首页> 美国卫生研究院文献>Evidence-based Complementary and Alternative Medicine : eCAM >Curcumin Suppresses Intestinal Fibrosis by Inhibition of PPARγ-Mediated Epithelial-Mesenchymal Transition
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Curcumin Suppresses Intestinal Fibrosis by Inhibition of PPARγ-Mediated Epithelial-Mesenchymal Transition

机译：姜黄素通过抑制PPARγ介导的上皮-间质转化抑制肠道纤维化

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摘要

Intestinal fibrotic stricture is a major complication of Crohn's disease (CD) and epithelial-to-mesenchymal transition (EMT) is considered as an important contributor to the formation of intestinal fibrosis by increasing extracellular matrix (ECM) proteins. Curcumin, a compound derived from rhizomes of Curcuma, has been demonstrated with a potent antifibrotic effect. However, its effect on intestinal fibrosis and the potential mechanism is not completely understood. Here we found that curcumin pretreatment significantly represses TGF-β1-induced Smad pathway and decreases its downstream α-smooth muscle actin (α-SMA) gene expression in intestinal epithelial cells (IEC-6); in contrast, curcumin increases expression of E-cadherin and peroxisome proliferator-activated receptor γ (PPARγ) in IEC-6. Moreover, curcumin promotes nuclear translocation of PPARγ and the inhibitory effect of curcumin on EMT could be reversed by PPARγ antagonist GW9662. Consistently, in the rat model of intestinal fibrosis induced by 2,4,5-trinitrobenzene sulphonic acid (TNBS), oral curcumin attenuates intestinal fibrosis by increasing the expression of PPARγ and E-cadherin and decreasing the expression of α-SMA, FN, and CTGF in colon tissue. Collectively, these results indicated that curcumin is able to prevent EMT progress in intestinal fibrosis by PPARγ-mediated repression of TGF-β1/Smad pathway.
机译：肠纤维化狭窄是克罗恩病（CD）的主要并发症，上皮到间质转化（EMT）被认为是通过增加细胞外基质（ECM）蛋白来形成肠纤维化的重要因素。姜黄素是一种源自姜黄根茎的化合物，具有有效的抗纤维化作用。但是，其对肠道纤维化的作用及其潜在机制尚未完全了解。在这里，我们发现姜黄素预处理可显着抑制TGF-β1诱导的Smad通路并降低其在肠上皮细胞（IEC-6）中的下游α-平滑肌肌动蛋白（α-SMA）基因表达；相反，姜黄素可提高IEC-6中E-钙粘蛋白和过氧化物酶体增殖物激活受体γ（PPARγ）的表达。此外，姜黄素促进PPARγ的核易位，而姜黄素对EMT的抑制作用可被PPARγ拮抗剂GW9662逆转。一致地，在2,4,5-三硝基苯磺酸（TNBS）诱导的大鼠肠纤维化模型中，口服姜黄素通过增加PPARγ和E-钙粘蛋白的表达并降低α-SMA，FN，和结肠组织中的CTGF。总体而言，这些结果表明姜黄素能够通过PPARγ介导的TGF-β1/ Smad通路的抑制来阻止肠纤维化的EMT进展。

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