WANG Chang-ming, CHEN Juan, JIANG Ming, XUAN Xiu-ping, LI Hong-xiu. Relationship between artesunate influence on the process of TGF-β1 induced alveolar epithelial cells transform into mesenchymal cells and on idiopathic pulmonary fibrosisJ. Acta Pharmaceutica Sinica, 2014,49(1): 142-147.
Citation: WANG Chang-ming, CHEN Juan, JIANG Ming, XUAN Xiu-ping, LI Hong-xiu. Relationship between artesunate influence on the process of TGF-β1 induced alveolar epithelial cells transform into mesenchymal cells and on idiopathic pulmonary fibrosisJ. Acta Pharmaceutica Sinica, 2014,49(1): 142-147.

Relationship between artesunate influence on the process of TGF-β1 induced alveolar epithelial cells transform into mesenchymal cells and on idiopathic pulmonary fibrosis

  • This study is to investigate the effect of artesunate on transforming growth factor-β1 (TGF-β1) induced epithelial-mesenchymal transition (EMT) and its possible mechanism. After the in vitro cultured RLE-6TN cells were treated with TGF-β1 then artesunate intervened on it, after 24 h, expression of the markers of mesenchymal cell was assayed using Western blotting and real-time PCR analysis. Western blotting was also used to detect the effect of TGF-β1 on the Smad3 and Smad7 expressions of RLE-6TN cells. Morphological alterations were examined by phase-contrast microscope, and ultrastructure changes by electron microscope. Incubation of RLE-6TN cells with TGF-β1 resulted in the up-regulation of the expression of the mesenchymal cell markers, after artesunate intervened on it, resulted in the down-regulation of the expression. Meanwhile, incubation with artesunate intervened on RLE-6TN cells could lead to the apparent down-regulation of the expression of Smad3 and up-regulation of Samd7 and the transition of RLE-6TN cells to mesenchymal-like by TGF-β1 induction, after artesunate intervened on it, RLE-6TN cells to epithelial-like. TGF-β1 induced epithelial-mesenchymal transition process; artesunate can inhibit TGF-β1-induced epithelial-mesenchymal transition process, the possible mechanism is up-regulation of the expression of Smad7 and down-regulation of the expression of Smad3, meanwhile inhibits phosphorylation of Smad3.
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