%A Lü Ya-nan, GU Qing, LI Dong-li, GONG Yuan-yuan %T Effects of lutein on transforming growth factor-&beta;2 induced epithelial-mesenchymal transition in ARPE-19 cells %0 Journal Article %D 2019 %J Journal of Shanghai Jiao Tong University (Medical Science) %R 10.3969/j.issn.1674-8115.2019.06.003 %P 571- %V 39 %N 6 %U {https://xuebao.shsmu.edu.cn/CN/abstract/article_12252.shtml} %8 2019-06-28 %X Objective · To establish the transforming growth factor-β2 (TGF-β2) induced epithelial-mesenchymal transition (EMT) model of retinal pigment epithelium cells, and investigate the effect and mechanism of lutein on EMT. Methods · ARPE-19 cells were cultured and divided into 4 groups including control group, TGF-β2 group, TGF-β2+lutein group and lutein group. The mRNA levels of α-smooth muscle actin (α-SMA), fibronectin (FN) and E-cadherin were analyzedreal-time PCR. The protein of α-SMA, FN and occludin were assayedWestern blotting. Immunofluorescence was used to detect the change of α-SMA. Meanwhile, Western blotting was performed to detect the levels of pSmad3 in the TGF/Smad signaling pathway. Results · TGF-β2 induced EMT was inhibitedlutein. Lutein decreased the mRNA and protein levels of the mesenchymal markers α-SMA and FN, and increased the of the epithelial markers E-cadherin and occludin (all P<0.05). Immunofluorescence showed that lutein can inhibit the conversion of epithelial cells into myofibroblasts. Lutein significantly downregulated the high of pSmad3 in TGF-β2 treated ARPE-19 cells (P0.001). Conclusion · Lutein inhibits TGF-β2 induced EMTdownregulating the of pSmad3 in TGF-β/ Smad signaling pathway, indicating it may attenuate subretinal fibrosis.