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. Epub 2017 Aug 31.


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.

MeSH terms

  • Cell Adhesion / drug effects
  • E-Selectin / analysis
  • E-Selectin / genetics
  • E-Selectin / metabolism
  • Enzyme-Linked Immunosorbent Assay
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Indoles / chemistry
  • Indoles / pharmacology*
  • Inflammation / prevention & control*
  • Intercellular Adhesion Molecule-1 / analysis
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / metabolism
  • Interleukin-8 / metabolism
  • RNA, Messenger / metabolism
  • Reactive Oxygen Species / metabolism
  • Thiocarbamates / chemistry
  • Thiocarbamates / pharmacology*
  • Transcription Factor RelA / antagonists & inhibitors
  • Transcription Factor RelA / metabolism
  • Tumor Necrosis Factor-alpha / toxicity*
  • U937 Cells
  • Vascular Cell Adhesion Molecule-1 / analysis
  • Vascular Cell Adhesion Molecule-1 / genetics
  • Vascular Cell Adhesion Molecule-1 / metabolism


  • E-Selectin
  • Indoles
  • Interleukin-8
  • RNA, Messenger
  • Reactive Oxygen Species
  • Thiocarbamates
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • brassinin
  • Intercellular Adhesion Molecule-1