期刊
INFLAMMATION
卷 35, 期 2, 页码 584-593出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-011-9349-x
关键词
vitexicarpin; adhesion molecule; HUVEC; inflammation; NF-kappa B
资金
- National Research Foundation of Korea (NRF)
- Korea government (MEST) [2010-0029465, K10040]
- Korea Institute of Oriental Medicine
- National Research Council of Science & Technology (NST), Republic of Korea [K10040] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Pro-inflammatory cytokines induce injury of endothelial cells caused by increases of adhesion molecules, leading to vascular inflammation and the development of atherosclerosis. Recent pharmacological studies have demonstrated that vitexicarpin, a flavonoid isolated from Vitex rotundifolia, has anti-inflammatory, antitumor, and analgesic properties. In this study, we investigated whether vitexicarpin (5-100 nM) prevented the TNF-alpha-induced vascular inflammation process in human umbilical vein endothelial cells (HUVEC). We found that pretreatment with vitexicarpin decreased TNF-alpha (10 ng/ml)-induced expression of cell adhesion molecules such as vascular cell adhesion molecule-1, intracellular adhesion molecule-1, and E-selectin as well as matrix metalloproteinase-2 and -9 expression. Preincubation with vitexicarpin also dose-dependently inhibited TNF-alpha-induced adhesion of HL-60 monocytic cells. Vitexicarpin significantly decreased TNF-alpha-induced intracellular reactive oxygen species (ROS) production. Furthermore, vitexicarpin suppressed NF-kappa B nuclear translocation and transcriptional activity in TNF-alpha-treated HUVEC. In conclusion, vitexicarpin significantly reduced vascular inflammation, through inhibition of ROS-NF-kappa B pathway in vascular endothelial cells.
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