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

Yan,Li‑Jie; Yang,Hai‑Tao; Duan,Hong‑Yan; Wu,Jin‑Tao; Qian,Peng; Fan,Xian‑Wei; Wang,Shanling

doi:10.3892/mmr.2017.7321

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

Authors:
- Li‑Jie Yan
- Hai‑Tao Yang
- Hong‑Yan Duan
- Jin‑Tao Wu
- Peng Qian
- Xian‑Wei Fan
- Shanling Wang
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Affiliations: Department of Cardiology, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China
Published online on: August 22, 2017 https://doi.org/10.3892/mmr.2017.7321
Pages: 6354-6359

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Abstract

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‑α (TNF‑α)‑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‑α‑stimulated mouse MOVAS‑1 VSMC cells, and reduced the expression of adhesion molecules in TNF‑α‑stimulated MOVAS‑1 cells. In addition, myricitrin significantly inhibited the TNF‑α‑induced expression of nuclear factor (NF)‑κB p65, and prevented the TNF‑α‑induced degradation of nuclear factor of κ light chain enhancer in B‑cells inhibitor α. Furthermore, myricitrin inhibited the production of intracellular reactive oxygen species in TNF‑α‑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‑α‑stimulated MOVAS‑1 cells potentially via the NF‑κB signaling pathway. Therefore, myricitrin may be an effective pharmacological agent for the prevention or treatment of atherosclerosis.

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