XXXX inhibits lipid peroxidation-induced adhesion molecule expression in endothelial cells and decreases soluble cell adhesion molecules in healthy subjects.

@entity1 @entity32 @entity274 @entity270 @entity310 @entity1881
OBJECTIVE: In a combination of in vivo and in vitro studies, we investigated mechanisms via which @entity1881 , a lipid soluble form of @entity270 , can directly affect endothelial activation as induced by @entity274 and @entity310 . METHODS: We measured effects of @entity1881 on @entity274 -induced lipid peroxidation as determined with a fluorescent C-11 BODIPY(581/591) probe and on adhesion molecule expression in cultured endothelial cells. In 20 healthy volunteers treated with increasing doses of @entity1881 up to 800 IU/ml for 12 weeks, plasma levels of soluble cell adhesion molecules (sCAMs) and C-reactive protein were measured. RESULTS: We showed that @entity1881 protects cultured endothelial cells against @entity274 -induced lipid peroxidation, while @entity310 did not induce lipid peroxidation. Moreover, @entity1881 attenuated @entity274 -, but not @entity310 -induced increases in adhesion molecule expression. In healthy @entity1 , @entity1881 decreased plasma levels of sE-selectin from 65+/-6 to 60+/-6 ng/ml (P=0.002), sVCAM from 893+/-31 to 853+/-23 ng/ml (P=0.022), and sICAM from 483+/-21 to 463+/-16 ng/ml (P=0.048). C-Reactive protein, as a sensitive marker of low grade @entity32 , was not significantly affected. CONCLUSION: @entity1881 specifically inhibits lipid peroxidation-induced endothelial activation in vitro. The observed @entity270 -induced decrease in sCAMs in control subjects suggests that lipid peroxidation can take place in healthy individuals. Although @entity270 supplementation may be especially effective in specific groups of @entity1 exposed to increased oxidative stress, our study suggests that @entity270 supplementation can be of benefit in healthy individuals as well.
