Mechanism of Quercetin Mediating PI3K/Akt/mTOR Pathway in Alleviating Cerebral Vascular Stenosis Caused by Vascular Endothelial Cell Injury

Di Wang, Nanliang Fu and Xichang Liu

Background and Objective: Venous stenosis can be accelerated by damage to vascular endothelial cells, which in turn leads to the ischemic death of brain cells such as cerebrovascular endothelial cells. This study explored the impact of Quercetin (Que) on the physiological responses of human brain microvascular endothelial cells (HBVECs) to oxygen-glucose deprivation (OGD). Materials and Methods: The HBVECs were randomly divided into Control group (CG, conventional culture), OGD group (OGDG), Que-5, 10 and 20 (supplemented with 5, 10 or 20 μmol/L Que). Cell proliferation, apoptosis, inflammation and oxidative damage factors and the expression of PI3K/Akt/mTOR pathway proteins were detected. The SNK-q test and One-way Analysis of Variance (ANOVA) were adopted (p-value below 0.05). Results: With the increase of Que concentration, DPPH and ABTS free radical (FR) scavenging rate (SR) increased. As against the CG, in the OGDG, the cell survival rate (CSR) dropped while the apoptosis rate (AR) rose; TNF-α, IL-6 and IL-1β, oxidative stress (OS) factors ROS, MDA and 8-OHdG were increased and SOD was decreased; damage genes VCAM-1, ICAM-1 and EDN-1 was increased; Bax, Caspase-3, p-PI3K, p-Akt and p-mTOR rose visibly and Bcl-2 dropped. However, when the Que group (QG) was compared with the OGDG, a reverse trend was observed (all p<0.05). The changes in cell biological behavior after Que treatment were concentration-dependent. Conclusion: The Que has antioxidant properties and can promote proliferation, inhibit apoptosis, improve inflammation and OS and alleviate cell damage in HBVECs cell injury model induced by OGD.

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