Protective effects of isorhamnetin on apoptosis and inflammation in TNF-α-induced HUVECs injury

Little is known about the role of isorhamnetin on endothelial cell apoptosis and inflammation when insulted by TNF-alpha injury. In our study, HUVECs were treated with TNF-alpha for 6 hours. HUVECs apoptosis were detected using flow cytometry. The expressions of ICAM-1, VCAM-1, E-selectin, NF-kappa B, AP-1 and eNOS were determined with western blotting or flow cytometry. The results showed TNF-alpha increased of apoptosis and the expression of ICAM-1, VCAM-1 and E-selectin in HUVECs, accompanied by significant augmentation of NF-kappa B and AP-1 expression. Pretreatment with isorhamnetin significantly reduced apoptosis in TNF-alpha-treated HUVECs. Moreover, isorhamnetin significantly attenuated TNF-alpha-induced upregulation of ICAM-1, VCAM-1, AP-1, E-selectin and NF-kappa B expression. Meanwhile, isorhamnetin also increased the expression of eNOS. So, isorhamnetin could suppress TNF-alpha-induced apoptosis and inflammation by blocking NF-kappa B and AP-1 signaling in HUVECs, which might be one of the underlying mechanisms for treatment of coronary heart disease.