Abstract: 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.

Key words: subretinal fibrosis, lutein, transforming growth factor-&, beta, 2 (TGF-&, beta, 2), epithelial-mesenchymal transformation (EMT), retinal pigment epithelium cell (RPE)