摘要
This study aimed to explore the effect of DT-13 （25（R,S）-ruscogenin- 1-O- [ β-d-glucopyranosyl- （1→2） ] [ β-d-xylopyranosyl-（ 1→3） 1-β -d- fucopyranoside） on tumor necrosis factor （TNF）-α-induced vascular inflamma- tion and the potential molecular mechanisms. In vitro, DT-β suppressed TNF-α-induced adhesion and migration of human umbilical vein endothelial cells （HUVECs） by inhibiting the expression of intercellular adhesion molecule-1 （ ICAM-1 ） and vascular cell adhesion molecule-1 （VCAM-1）. DT-β markedly suppressed NF-KB p65 phosphoryl- ation, and when NF-KB p65 was over-expressed, the inhibitory effect of DT-β on adhesion molecular decreased. DT-β also suppressed TNF-α induced luciferase activities of ICAM-1 and VCAM-1 promoter containing NF-KB binding sites. Furthermore DT-β markedly suppressed p38 phosphorylation and Src degradation induced by TNF-α DT-β at 4 mg·kg- 1 prevented vascular , whereas had no significant effect on ERK and JNK activation. In-vivo, inflammation and the expression of adhesion molecules induced by TNF-α in mice. These findings suggest that DT- β abrogates vascular inflammation by down-regulating adhesion molecules associated with modulating the NF-KB, p38MAPK, Src signaling pathways, and NF-KB binding site is at least one of the targets of DT-β. This study pro- vides novel information regarding the mechanism by which DT-β exerts its effects on vascular inflammation, which is important for the onset and progression of various diseases.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2015年第B11期197-198,共2页
Chinese Pharmacological Bulletin
