Abstract: Objective To demonstrate whether EPO can inhibit Müller cell apoptosis induced by oxidative damage and to investigate the molecular mechanism. Methods The proliferation effect of EPO on cultured human Müller cell-MIO-M1 was determined by BrdU marking and MTT assay both under normal condition and exposed to H₂O₂ or GO with different concentration (0 U/mL, 0.01 U/mL, 0.1 U/mL, 1 U/mL, 10 U/mL, 30 U/mL and 100 U/mL) at 24 h, 48 h and 72 h after exposure. The Müller cell proliferation changes after the use of PI3K/PDK1/PKB(Akt) signal pathway blocker-LY294002 was surveyed by MTT assay. The Müller cell function on EPO expression and secretion was observed by ELISA. The EPO effect on ERK1/2 and Akt signal pathway was detected under different cultured condition in vitro by Western-blotting. Results EPO had no effect on Müller cell proliferation under normal culture condition. The 80% damaged Müller cell caused by 0.4 mmol/L H₂O₂ can secrete 1.42 times EPO as that under normal culture condition. Under oxidative damage condition, 0.08 mmol/L H₂O₂ or 8 U/L GO could cause half of Müller cells to be dead and activate Akt signal pathway. While adding EPO 2 h earlier, 30 U/mL of EPO can reduce the oxidative damage to the minimum. The protection effect of Akt signal pathway could be reduced by its blocker LY294002 spontaneously. Conclusion EPO has no proliferation and migration effects on Müller cells cultured in vitro. Under normal culture condition, Müller cells did not express and secrete EPO. While under oxidative damage, Müller cells can secret EPO which can protect Müller cells by Akt signal pathway.

Key words: ller cells, Age-related macular degeneration, Mü, Erythropoietin, Proliferation