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

Darkhan I. Utepbergenov, Katharina Mertsch, Anje Sporbert, Kareen Tenz, Martin Paul, Reiner F. Haseloff, Ingolf E. Blasig

Research output: Contribution to journalArticlepeer-review

86 Citations (Scopus)

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 μM), authentic .NO (6 μM) or superoxide dismutase (50 units/ml) during H/R attenuated H/R-induced increase in permeability. 30 μM SNAP or 6 μM .NO did not influence the function of BBB during normoxia, however, severe disruption was observed using 150 μM of SNAP and more than 24 μM 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 μM SNAP or 6 μM 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.

Original languageEnglish
Pages (from-to)197-201
Number of pages5
JournalFEBS Letters
Volume424
Issue number3
DOIs
Publication statusPublished - Mar 13 1998

Keywords

  • Blood-brain barrier
  • Endothelial cell
  • Hypoxia
  • Lipid peroxidation
  • Nitric oxide
  • Oxygen radical

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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