The protective effect of quercetin on vascular endothelial progenitor cells by regulating PI3K/AKT signaling pathway and its mechanisms / 中国药理学通报

ABSTRACT

Aim To study the protective effect of quercetin ( Que) on vascular endothelial progenitor cells ( EPCs) under oxidative stress and the underlying mechanisms. Methods The human umbilical cord blood EPCs were separated .differentiated and randomized into two groups, namely, hydrogen peroxide (H202) group, in which the oxidative stress damage EPCs model was established by adding H202 of 500 jjunol • L"1 ,and Que intervention group,in which Que pretreated with a concentration of 60 jimol • L~' and 90 p.mol • L'1 was added for 30 min respectively, and then 500 jimol • L"1 H202 was added for co-culture. WST-1 method was used to assess the proliferation of EPCs after 12,24 and 48 h culture. Western blot was used to detect the expression levels of Akt and phos- phorylated Akt. Real-time fluorescence RT-PCR was employed to determine the expression levels of PI3K and AKT3 mRNA. Results Compared with blank control group,the proliferation capacity of EPCs treated with hydrogen peroxide was significantly reduced. The expression of Akt protein in EPCs decreased significantly, and the relative expression of PI3K and AKT3 mRNA decreased significantly ( P < 0. 01, P < 0. 05 ). After 60,90 jtmol • L"1 Que was added for 12,24 and 48 h,respectively,the proliferation capacity of damaged EPCs cells increased significantly, and the difference was statistically significant compared with the model group (fcO. 05). At the same time, the protein expression of p-Akt in EPCs significantly increased ( P < 0.05),and mRNA expression of PI3K and AKT3 increased ( P < 0. 01 ). Conclusions Que can fix the EPCs oxidative stress induced by H202 ,and its mecha-nism may be through the activation of PI3K/AKT signaling pathway, reducing the influence of oxidative stress on cerebrovascular lesions,and promoting the proliferation and differentiation of cerebrovascular EPCs.