Affiliations: First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kamigyo‐ku, Kyoto 602, Japan
Note: [] Address for correspondence: Toshikazu Yoshikawa, First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kawaramachi‐Hirokoji, Kamigyo‐ku, Kyoto 602, Japan. Fax: +81 75 252 3721.
Abstract: Leukocyte–endothelial cell interactions, which are mediated by various adhesion molecules, are a crucial event in inflammatory reactions including atherosclerosis. \alpha‐tocopherol (\alpha‐Toc) has been used for therapy of vascular diseases because of its antioxidant activity. However, the effect of \alpha‐Toc on inflammatory reactions has not been investigated very well. In the present study, we examined the effect of \alpha‐Toc on expression of adhesion molecules on human neutrophils and human umbilical vein endothelial cells (HUVEC). Expression of CD11a, CD11b and CD18 on neutrophils was assessed by immunofluorescence flow cytometry 30 min after the stimulation of neutrophils with 10^{-7} M platelet‐activating factor (PAF). Surface expression of intercellular adhesion molecule‐1 (ICAM‐1) and vascular cell adhesion molecule‐1 (VCAM‐1) on HUVEC was evaluated by enzyme immunoassay 8 h after the incubation of HUVEC with IL‐1\beta (20 U/ml). PAF induced upregulation of CD11b and CD18 on neutrophils and IL‐1\beta increased surface expression of ICAM‐1 and VCAM‐1 on HUVEC. Coincubation of neutrophils with \alpha‐Toc and pretreatment of HUVEC with \alpha‐Toc significantly reduced PAF‐induced CD11b/CD18 expression and IL‐1\beta‐induced upregulation of ICAM‐1 and VCAM‐1, respectively. These findings indicate that \alpha‐Toc may work as an anti‐inflammatory agent through inhibiting neutrophil–endothelial cell adhesive reactions.
