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Poster Session : PS 1582 ; DILD : Sulforaphane Attenuates TGF-ß-Induced Fibrosis and Alveolar Epithelial to Mesenchymal Transition
( Sun Young Kyung ) , ( Jin Young Yoon ) , ( Sang Min Lee ) , ( Shin Myung Kang ) , ( Yu Jin Kim ) , ( Sang Pyo Lee ) , ( Jeong Woong Park ) , ( Sung Hwan Jeong )
UCI I410-ECN-0102-2015-500-000137313
이 자료는 4페이지 이하의 자료입니다.

Background: Sulforaphane(SF) is a isothiocyanate that has anti-infi ammatory effect via induction of antioxidant/phase II enzymes. We evaluated the effects of SF on pulmonary fi brosis and alveolar epithelial to mesenchymal transition (EMT). Methods: Western blotting for fi bronectin, collagen, total/phosphorylated smad2/3, 7 was evaluated in TGF-ß-treated pulmonary fi broblast cells (MRC-5 cells) with or without SF. In alveolar epithelial cells (A549 cells), morphological changes induced byTGF-ß was observed with or without SF. And then Western blotting for E-cadherin, vimentin, a-Smooth muscle actin (SMA) and quantitative real-time PCR were evaluated for transcriptional factors: Slug, Snail, and Twist. Results: SF attenuates TGF-ß-induced fi bronectin and collagen protein production in pulmonary fi broblasts. Furthermore, SF showed relation to smad 2/3 and smad 7 phosphorylation. In A549 cells, we observed TGF-ß-induced alveolar EMT by morphological changes, decreased E-cadherin expression, increased expression of vimentin and a-SMA. These alveolar EMT was inhibited by SF treatment related to inhibiting Snail, Slug, and Twist. Conclusions: SF has anti-fi brotic potential in pulmonary fi brosis which attenuates the expression of fi brogenic proteins via TGF-ß-smad signaling and inhibits alveolar EMT.

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