【摘 要】
：
This study aimed to explore the effect of DT13 (25(R,S)ruscogenin10βdglucopyranosyl(1→2)][βdxylopyranosyl(1→3)]βdfucopyranoside) on tumor necrosis factor (TNF)αinduced vascular inflammation and the po
【机 构】
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Jiangsu Key Laboratory of TCM Evaluation and Translational Research,Department of Complex Prescripti
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This study aimed to explore the effect of DT13 (25(R,S)ruscogenin10βdglucopyranosyl(1→2)][βdxylopyranosyl(1→3)]βdfucopyranoside) on tumor necrosis factor (TNF)αinduced vascular inflammation and the potential molecular mechanisms.In vitro, DT13 suppressed TNFαinduced adhesion and migration of human umbilical vein endothelial cells (HUVECs) by inhibiting the expression of intercellular adhesion molecule1(ICAM1) and vascular cell adhesion molecule1 (VCAM1).DT13 markedly suppressed NFκB p65 phosphorylation, and when NFκB p65 was overexpressed, the inhibitory effect of DT13 on adhesion molecular decreased.DT13 also suppressed TNFα induced luciferase activities of ICAM1 and VCAM1 promoter containing NFκBbinding sites.Furthermore, DT13 markedly suppressed p38 phosphorylation and Src degradation induced by TNFo, whereas had no significant effect on ERK and JNK activation.In vivo, DT13 at 4 mg · kg1 prevented vascular inflammation and the expression of adhesion molecules induced by TNFα in mice.These findings suggest that DT13 abrogates vascular inflammation by downregulating adhesion molecules associated with modulating the NFκB,p38MAPK, Src signaling pathways, and NFκB binding site is at least one of the targets of DT13.This study provides novel information regarding the mechanism by which DT13 exerts its effects on vascular inflammation, which is important for the onset and progression of various diseases.
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