Inhibitory effect of brassinin on TNF‑α‑induced vascular inflammation in human umbilical vein endothelial cells

  • Mol Med Rep. 2017 Nov;16(5):6890-6895. doi: 10.3892/mmr.2017.7406.
Byung Hyuk Han  1 ,  Jung Joo Yoon  1 ,  Eun Sik Choi  1 ,  Da Hye Jeong  1 ,  Yun Jung Lee  1 ,  Dae Gill Kang  1 ,  Ho Sub Lee  1
Affiliations
  • 1. College of Oriental Medicine and Professional Graduate School of Oriental Medicine, Wonkwang University, Iksan, Jeonbuk 54538, Republic of Korea.
Abstract

Brassinin, a phytoalexin firstly identified as a constituent of Chinese cabbage, has been demonstrated to exhibit antiproliferative effects on various Cancer cell lines, by reducing reactive oxygen species (ROS) production via regulation of the antioxidant pathway. The present study aimed to explore the protective effects of brassinin in TNF‑α‑induced vascular inflammation in human umbilical vein endothelial cells (HUVECs). Pretreatment with brassinin significantly inhibited adhesion of U937 cells to TNF‑α‑induced HUVECs in a dose‑dependent manner. Brassinin treatment decreased the expression levels of cell adhesion molecules, including intracellular adhesion molecule‑1 (ICAM‑1), vascular cell adhesion molecule‑1 (VCAM‑1), and endothelial‑selectin (E‑selectin) following stimulation with TNF‑α in HUVECs. In addition, pretreatment with brassinin decreased the protein expression levels of nuclear factor (NF)‑κB p65 in the nucleus, suggesting that brassinin inhibited NF‑κB p65 nuclear translocation. Brassinin treatment also markedly decreased the mRNA expression levels of interleukin‑8 in a dose‑dependent manner. Finally, brassinin pretreatment significantly decreased TNF‑α‑induced intracellular reactive oxygen species (ROS) production in HUVECs compared with control. The present results therefore suggest that brassinin may serve as a potential therapeutic agent for Atherosclerosis.