Quercetin inhibits TNF-α induced HUVECs apoptosis and inflammation via downregulating NF-kB and AP-1 signaling pathway in vitro.
Quercetin inhibits TNF-α induced HUVECs apoptosis and inflammation via downregulating NF-kB and AP-1 signaling pathway in vitro.
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DOI：
10.1097/md.0000000000022241
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发表时间：
2020-09-18
期刊：
影响因子：
1.6
通讯作者：
He X
中科院分区：
文献类型：
--
作者：
Chen T;Zhang X;Zhu G;Liu H;Chen J;Wang Y;He X
槲皮素是植物中广泛存在的一种重要的黄酮醇，具有抗血管内皮细胞凋亡和抗炎的作用，但其分子机制尚不清楚。本研究旨在探讨槲皮素抑制肿瘤坏死因子-α诱导人脐静脉内皮细胞凋亡和炎症的机制。用槲皮素预处理HUVEC 18 h，再用肿瘤坏死因子-α处理6 h诱导细胞凋亡。逆转录-聚合酶链式反应检测细胞间黏附分子-1、血管细胞黏附分子-1、E-选择素、β-肌动蛋白的表达。流式细胞仪检测细胞凋亡率，Western印迹法检测细胞中活化蛋白1(AP-1)和核因子-kappaB(NF-κB)的表达。α诱导的人脐静脉内皮细胞凋亡率增加，细胞间黏附分子-1、E-选择素的表达明显降低。此外，槲皮素还可抑制AP-1和NF-κB的活化。结果表明，槲皮素通过阻断NF-αB和AP-1信号通路抑制肿瘤坏死因子-κ诱导的内皮细胞的凋亡和炎症反应，这可能是其治疗冠心病的机制之一。
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.