Nitric oxide protects blood-brain barrier in vitro from hypoxia/reoxygenation-mediated injury.

Abstract:

:A cell culture model of blood-brain barrier (BBB, coculture of rat brain endothelial cells with rat astrocytes) was used to investigate the effect of nitric oxide (.NO) on the damage of the BBB induced by hypoxia/reoxygenation (H/R). Permeability coefficient of fluorescein across the endothelium was used as a marker of BBB tightness. The permeability coefficient increased 5.2 times after H/R indicating strong disruption of the BBB. The presence of the .NO donor S-nitroso-N-acetylpenicillamine (SNAP, 30 microM), authentic .NO (6 microM) or superoxide dismutase (50 units/ml) during H/R attenuated H/R-induced increase in permeability. 30 microM SNAP or 6 microM .NO did not influence the function of BBB during normoxia, however, severe disruption was observed using 150 microM of SNAP and more than 24 microM of .NO. After H/R of endothelial cells, the content of malondialdehyde (MDA) increased 2.3 times indicating radical-induced peroxidation of membrane lipids. 30 microM SNAP or 6 microM authentic .NO completely prevented MDA formation. The results show that .NO may effectively scavenge reactive oxygen species formed during H/R of brain capillary endothelial cells, affording protection of BBB at the molecular and functional level.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Utepbergenov DI,Mertsch K,Sporbert A,Tenz K,Paul M,Haseloff RF,Blasig IE

doi

10.1016/s0014-5793(98)00173-2

subject

Has Abstract

pub_date

1998-03-13 00:00:00

pages

197-201

issue

3

eissn

0014-5793

issn

1873-3468

pii

S0014-5793(98)00173-2

journal_volume

424

pub_type

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