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Inhibitory effects of vitamin E on endothelial‐dependent adhesive interactions with leukocytes induced by oxidized low density lipoprotein
Author(s) -
Yoshida N.,
Manabe H.,
Terasawa Y.,
Nishimura H.,
Enjo F.,
Nishino H.,
Yoshikawa T.
Publication year - 2000
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520130142
Subject(s) - chemistry , cell adhesion molecule , adhesion , lipoprotein , monoclonal antibody , endothelial stem cell , intracellular , cell adhesion , intercellular adhesion molecule 1 , vitamin e , icam 1 , low density lipoprotein , biochemistry , microbiology and biotechnology , pharmacology , antioxidant , antibody , cell , in vitro , immunology , cholesterol , biology , organic chemistry
Abstract Leukocyte‐endothelial cell interactions, which are mediated by various adhesion molecules, are a crucial event in inflammatory reactions including atherosclerosis. α‐Tocopherol (α‐Toc) has been used for protection and therapy of vascular diseases because of its antioxidant activity. The objective of the present study was to determine effect of α‐Toc on endothelial‐dependent adhesive interactions with leukocytes elicited by oxidized low density lipoprotein (oxLDL). Incubation of HUVEC with oxLDL (100 μg/mL) increased expression of proteins and messenger RNA of intercellular adhesion molecule‐1 (ICAM‐1) and vascular cell adhesion molecule‐1 (VCAM‐1) on enzyme immunoassay and northern blotting assay; pretreatment with α‐Toc reduced in a dose dependent manner. Adherence of polymorphonuclear leukocytes (PMN) or mononuclear leukocytes (MNC) to oxLDL‐activated HUVEC was much increased compared with that to unstimulated HUVEC. Treatment of HUVEC with α‐Toc, monoclonal antibody to ICAM‐1 or VCAM‐1 inhibited adherence of PMN or MNC in a dose dependent manner. These results suggest that α‐Toc works as anti‐atherogenic agent through inhibiting endothelial‐dependent adhesive interactions with leukocytes induced by oxLDL.