Quercetin inhibits TNF-α induced HUVECs apoptosis and inflammation via downregulating NF-kB and AP-1 signaling pathway in vitro

• Published in: Medicine (Baltimore) Vol. 99; no. 38; p. e22241
• Main Authors: Chen, Tielong, Zhang, Xudong, Zhu, Guangli, Liu, Hongfei, Chen, Jinru, Wang, Yu, He, Xiaolong
• Format: Journal Article
• Language: English
• Published: United States Lippincott Williams & Wilkins 18.09.2020
• Subjects: Anti-Inflammatory Agents - pharmacology; Apoptosis - drug effects; Clinical Trial/Experimental Study; Down-Regulation; E-Selectin - metabolism; Human Umbilical Vein Endothelial Cells - cytology; Humans; Inflammation - metabolism; Inflammation - pathology; Inflammation - prevention & control; Intercellular Adhesion Molecule-1 - metabolism; NF-kappa B - metabolism; Quercetin - pharmacology; Signal Transduction; Transcription Factor AP-1 - metabolism; Tumor Necrosis Factor-alpha - pharmacology; Vascular Cell Adhesion Molecule-1 - metabolism
• ISSN: 0025-7974; 1536-5964; 1536-5964
• DOI: 10.1097/MD.0000000000022241

Quercetin, a major flavonol, wildly exists in plantage, which has been reported to have an anti-apoptosis and anti-inflammation effects on vascular endothelial cells, but its underlying molecular mechanisms remain unclear. The aim of this study was to investigate the mechanisms of how quercetin inhibits tumor necrosis factor alpha (TNF-α) induced human umbilical vein endothelial cells (HUVECs) apoptosis and inflammation. HUVECs were preconditioned with quercetin for 18 hours, and subsequently treated with TNF-α for 6 hours to induce apoptosis. The expression of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), E-selectin, β-actin mRNA was then detected by RT-PCR. Flow cytometry was used to estimate the apoptosis rates, and the expression of activator protein 1 (AP-1) and nuclear factor kappa B (NF-κB) was measured by Western blot. TNF-α induced elevated apoptosis rates and upregulation of VCAM-1, ICAM-1, and E-selectin were meaningfully reduced in HUVECs by pretreatment with quercetin. In addition, quercetin also inhibited the activation of AP-1and NF-κB. Results indicate that quercetin could suppress TNF-α induced apoptosis and inflammation by blocking NF-κB and AP-1 signaling pathway in HUVECs, which might be one of the underlying mechanisms in treatment of coronary heart disease.