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

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87 Citations (Scopus)


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
Issue number3
Publication statusPublished - Mar 13 1998


  • 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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