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Aim To observe the protection of Pae on injuried VEC and the improvement of mgration and abnormal proliferation of SMC co-cultured with VECinduced by ox-LDL.To further clarify the relationship between the dysfunction of endothelial cells and SMC proliferation, migration,PI3K-AKT signaling pathway under the conditions of injuried VEC.Methods Establish co-culture system of SMC and VEC.To build VEC damage model, VEC were incubated with ox-LDL.The protection effects of Pae on impaired VEC induced by ox-LDL and the proliferation of SMC were detected by MTT.Transwell chamber was used for testing the role of VEC on SMC migration.The protein levels of VEGF、 PI3K、 AKT、 P-AKT were detected by Western blotting.Besides, the expression of PDGF-B、PCNA were disclosed by Immunohistochemistry.Results Pre-treated VEC with different concentrations of Pae (30,60,120 μ mol · L-1)for 24 h, which could significantly increase the survival rate of VEC;Pae has a maximum inhibition at 120 μ mol.L-1, 240 μ mol.L-1 for 24h;Pae (30,60,120 μ mol.L-1)for 24h could uncommonly reduce the proliferation of SMC co-cultured with impaired VEC induced by ox-LDL, and significantly lower the expression of PCNA of SMC;Pae (30, 60, 120 μ mol· L-1) could obviously inhibit the expression of PDGF-B、 VEGF of VEC;Pae(30, 60, 120μ mol ·L-1)could obviously let down the phosphorylation level of PI3K and AKT induced by ox-LDL.Conclusions It was obviousely that Pae could increase the survival rate of VEC which was decreased by ox-LDL,and that Pae could protect VEC from injuring induced by ox-LDL effectively.And Pae exerts the function of protecting injured VECs, which reduced VEGF, PDGF-B release of VECs and decreased PCNAexpression of VSMCs, prevented PI3K-AKT pathway activation and VSMCs overproliferation and migration.