Myricitrin inhibits vascular adhesion molecule expression in TNF-α-stimulated vascular smooth muscle cells

被引:11
作者
Yan, Li-Jie [1 ]
Yang, Hai-Tao [1 ]
Duan, Hong-Yan [1 ]
Wu, Jin-Tao [1 ]
Qian, Peng [1 ]
Fan, Xian-Wei [1 ]
Wang, Shanling [1 ]
机构
[1] Henan Prov Peoples Hosp, Dept Cardiol, 7 Weiwu Rd, Zhengzhou 450003, Henan, Peoples R China
关键词
atherosclerosis; myricitrin; adhesion molecule; vascular smooth muscle cells; NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; SIGNALING PATHWAYS; GENE-EXPRESSION; DOWN-REGULATION; HUMAN ATHEROSCLEROSIS; ENDOTHELIAL-CELLS; ICAM-1; EXPRESSION; MONOCYTE ADHESION; E-SELECTIN;
D O I
10.3892/mmr.2017.7321
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Increased expression of adhesion molecules is thought to serve an important role in the pathogenesis of atherosclerosis. Myricitrin, a bioactive compound of Myrica cerifera, has been demonstrated to exhibit anti-atherogenic effects. However, the effect of myricitrin on the expression of adhesion molecules in vascular smooth muscle cells (VSMCs) remains unknown. Therefore, the aim of the present study was to evaluate the inhibitory effects of myricitrin on tumor necrosis factor-alpha (TNF-alpha)-induced expression of adhesion molecules in VSMCs in vitro. The results revealed that myricitrin inhibited the adhesion of human THP-1 monocyte cells to TNF-alpha-stimulated mouse MOVAS-1 VSMC cells, and reduced the expression of adhesion molecules in TNF-alpha-stimulated MOVAS-1 cells. In addition, myricitrin significantly inhibited the TNF-alpha-induced expression of nuclear factor (NF)-kappa B p65, and prevented the TNF-alpha-induced degradation of nuclear factor of kappa light chain enhancer in B-cells inhibitor alpha. Furthermore, myricitrin inhibited the production of intracellular reactive oxygen species in TNF-alpha-stimulated MOVAS-1 cells. In conclusion, the results of the present study indicated that myricitrin inhibits the expression of vascular cell adhesion protein-1 and intercellular adhesion molecule-1 in TNF-alpha-stimulated MOVAS-1 cells potentially via the NF-kappa B signaling pathway. Therefore, myricitrin may be an effective pharmacological agent for the prevention or treatment of atherosclerosis.
引用
收藏
页码:6354 / 6359
页数:6
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