Thromb Haemost 1984; 51(01): 089-092
DOI: 10.1055/s-0038-1661027
Original Article
Schattauer GmbH Stuttgart

Protective Effect of Vitamin E on Immune Triggered, Granulocyte Mediated Endothelial Injury

M A Boogaerts
The University Hospital and Department of Medical Research, University Leuven, Belgium
,
J Van de Broeck
The University Hospital and Department of Medical Research, University Leuven, Belgium
,
H Deckmyn
The University Hospital and Department of Medical Research, University Leuven, Belgium
,
C Roelant
The University Hospital and Department of Medical Research, University Leuven, Belgium
,
J Vermylen
The University Hospital and Department of Medical Research, University Leuven, Belgium
,
R L Verwilghen
The University Hospital and Department of Medical Research, University Leuven, Belgium
› Author Affiliations
Further Information

Publication History

Received 27 January 1983

Accepted 23 November 1983

Publication Date:
19 July 2018 (online)

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Summary

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 <0.001).

The inhibition of PMN induced endothelial injury is directly correlated to a diminished adherence of PMN to vitamin E- cultured HUEC (p <0.001), which may be mediated by an increase of both basal and stimulated endogenous prostacyclin (PGI2) from alfa-tocopherol-treated HUEC (p <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.