AI Article Synopsis
- Brassinin, a phytoalexin found in Chinese cabbage, shows promise in reducing cancer cell growth by lowering reactive oxygen species (ROS) through the antioxidant pathway.
- In human umbilical vein endothelial cells (HUVECs), brassinin pretreatment inhibited the adhesion of U937 cells and reduced the expression of adhesion molecules like ICAM-1, VCAM-1, and E-selectin triggered by TNF-α.
- The study found that brassinin also decreased the nuclear presence of NF-κB p65 and reduced interleukin-8 mRNA levels, suggesting it could be a potential therapeutic agent for atherosclerosis by mitigating vascular inflammation.
Article 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.
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| http://dx.doi.org/10.3892/mmr.2017.7406 | DOI Listing |
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