Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/60401
標題: Eriodictyol decreases very late antigen-4 (VLA-4) expression, cellular adhesion, and migration through an NF kappa B-dependent pathway in monocytes
作者: Huang, T.C.
劉宏仁
Tseng, K.Y.
Tsai, S.S.
Liu, H.J.
Ho, C.T.
Lin, H.Y.
Cheng, L.T.
Chuang, K.P.
關鍵字: Eriodictyol;Leukocyte function;Very late antigen 4;Adhesion;Migration;NF kappa B;cells;molecules;integrin;atherosclerosis;flavonoids;inflammation;recruitment;activation;mechanisms
Project: Journal of Functional Foods
期刊/報告no:: Journal of Functional Foods, Volume 2, Issue 4, Page(s) 263-270.
摘要: 
Very late antigen 4 (VLA 4) mediated monocyte adhesion and transendothelial migration are important events during immune surveillance and in the pathogenesis of inflammatory diseases such as atherosclerosis Under physiological conditions, circulating monocytes that are in various states of maturation enter tissue microenvironments and participate in immune responses by interacting with other leukocytes The effects and regulatory mechanisms of eriodictyol on VLA 4 expression cell adhesion and migration in U937 cells were investigated Eriodictyol lowered VLA 4 expression in a dose and time dependent manner in U937 cells Moreover VLA 4 and vascular adhesion molecular 1 (VCAM 1) mediated adhesion and migration were decreased by eriodictyol Upon treatment with eriodictyol NF kappa B translocated to the nucleus the NF kappa B inhibitor JSH 23 inhibited this translocation and prevented the decrease of vLA 4 expression by eriodictyol Thus eriodictyol regulates immune responses by modulating VLA 4 expression, cellular migration, and VLA 4 mediated adhesion in monocytes - evidence that eriodictyol regulates adhesion molecules during immune responses (C) 2010 Elsevier Ltd All rights reserved
URI: http://hdl.handle.net/11455/60401
ISSN: 1756-4646
DOI: 10.1016/j.jff.2010.10.001
Appears in Collections:分子生物學研究所

Show full item record
 

Google ScholarTM

Check

Altmetric

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.