Tectorigenin protect HUVECs from HO-induced oxidative stress injury by regulating PI3K/Akt pathway.

Oxidative stress injury (OSI) occurs in many cardiovascular diseases, and the OSI of endothelial cells is the main pathological basis of these diseases. Tectorigenin has an effect on oxidative stress in fibroblasts, keratinocytes, and neuroblastoma. This study attempted to reveal the effect of Tectorigenin on OSI in endothelial cells. An OSI cell model was firstly established by treating human umbilical vein endothelial cells (HUVECs) with HO. The HO-induced HUVECs were further pre-treated with Tectorigenin or PI3K inhibitor. Then the viability and apoptosis of HUVECs were evaluated using MTT, Hochest 33258 staining and TUNEL staining. Lactate dehydrogenase (LDH) leakage, enzyme activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) level were measured through colorimetric assays. The expressions of apoptosis-related factors and the activation of the PI3K/Akt pathway in HUVECs were detected by RT-qPCR or Western blot. Tectorigenin had no inhibiting effect on the viability of HUVECs at the concentrations of 0.1, 0.5, 0.5, 1, and 10 μmol/L. Tectorigenin reversed the HO induced-destruction of HUVECs morphology. Tectorigenin increased the viability and decreased the apoptosis of HO-induced HUVECs. Tectorigenin increased Bcl-2 expression and the enzyme activities of SOD and GSH-Px, but decreased LDH leakage, MDA level, and the expressions of Bax and Cleaved Caspase-3 in HO-induced HUVECs. Furthermore, Tectorigenin increased the ratios of p-PI3K to PI3K and p-Akt to Akt in HO-induced HUVECs. PI3K inhibitor had an opposite effect of Tectorigenin on the OSI in HO-induced HUVECs and its effect was further reversed by Tectorigenin. Tectorigenin protected HUVECs against HO-induced OSI via PI3K/Akt pathway.