Protective effect of vitamin E on immune triggered, granulocyte mediated endothelial injury.
The effect of alfa-tocopherol on the cell-cell interactions at the vessel wall were studied, using an in vitro model of human umbilical vein endothelial cell cultures (HUEC). Immune triggered granulocytes (PMN) will adhere to and damage HUEC and platelets enhance this PMN mediated endothelial injury. When HUEC are cultured in the presence of vitamin E, 51Cr-leakage induced by complement stimulated PMN is significantly decreased and the enhanced cytotoxicity by platelets is completely abolished (p less than 0.001). The inhibition of PMN induced endothelial injury is directly correlated to a diminished adherence of PMN to vitamin E-cultured HUEC (p less than 0.001), which may be mediated by an increase of both basal and stimulated endogenous prostacyclin (PGI2) from alfa-tocopherol-treated HUEC (p less than 0.025). The vitamin E-effect is abolished by incubation of HUEC with the irreversible cyclo-oxygenase inhibitor, acetylsalicylic acid, but the addition of exogenous PGI2 could not reproduce the vitamin E-mediated effects. We conclude that vitamin E exerts a protective effect on immune triggered endothelial damage, partly by increasing the endogenous anti-oxidant potential, partly by modulating intrinsic endothelial prostaglandin production. The failure to reproduce vitamin E-protection by exogenously added PGI2 may suggest additional, not yet elucidated vitamin E-effects on endothelial metabolism.
D001241:Aspirin / Q000494:pharmacology; D002448:Cell Adhesion / Q000187:drug effects; D002450:Cell Communication / Q000187:drug effects*; D004727:Endothelium / Q000166:cytology* / Q000378:metabolism; D011464:Epoprostenol / Q000096:biosynthesis; D006098:Granulocytes / Q000166:cytology*; D006801:Humans; D007231:Infant, Newborn; D014810:Vitamin E / Q000494:pharmacology*
D014810:Vitamin E; D011464:Epoprostenol; D001241:Aspirin