ABSTRACT
We have demonstrated that α-tocopherol inhibits the expression of mRNA and protein for adhesion molecules by human umbilical vein endothelial cells (HUVEC) in response to stimulation with oxidized low-density lipoprotein (oxLDL) or interleukin (IL)-1 (Yoshikawa et al. 1998). In addition, we have shown in both in vitro and ex vivo studies that α-tocopherol decreases the expression of CD11b/CD18 on human monocytes induced by oxLDL (Yoshikawa et al. 1998; Terasawa et al. 2000; Yoshida et al. 2000). These data support the hypothesis that vitamin E supplementation may reduce the extent of the oxLDL-induced monocyte-endothelial interaction and, thus, be protective against atherosclerosis. This hypothesis may be supported by studies in murine models of atherosclerosis. In contrast, clinical trials using this vitamin have given a more confused picture than expected, with results ranging from a signicant protective action to the absence of any effect. A recent VEAPS study has demonstrated that α-tocopherol supplementation (dl-α-tocopherol 400 IU/ day) signicantly raises plasma vitamin E levels, reduces circulating oxLDL and reduces LDL oxidative susceptibility; the progression of the intima-media thickness of the common carotid artery, however, is not reduced by the treatment (Hodis et al. 2002).
