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 language | English |
|---|---|
| Pages (from-to) | 197-201 |
| Number of pages | 5 |
| Journal | FEBS Letters |
| Volume | 424 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Mar 13 1998 |
| Externally published | Yes |
Fingerprint
Keywords
- Blood-brain barrier
- Endothelial cell
- Hypoxia
- Lipid peroxidation
- Nitric oxide
- Oxygen radical
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Molecular Biology
Cite this
Nitric oxide protects blood-brain barrier in vitro from hypoxia/reoxygenation-mediated injury. / Utepbergenov, Darkhan I.; Mertsch, Katharina; Sporbert, Anje; Tenz, Kareen; Paul, Martin; Haseloff, Reiner F.; Blasig, Ingolf E.
In: FEBS Letters, Vol. 424, No. 3, 13.03.1998, p. 197-201.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Nitric oxide protects blood-brain barrier in vitro from hypoxia/reoxygenation-mediated injury
AU - Utepbergenov, Darkhan I.
AU - Mertsch, Katharina
AU - Sporbert, Anje
AU - Tenz, Kareen
AU - Paul, Martin
AU - Haseloff, Reiner F.
AU - Blasig, Ingolf E.
PY - 1998/3/13
Y1 - 1998/3/13
N2 - 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.
AB - 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.
KW - Blood-brain barrier
KW - Endothelial cell
KW - Hypoxia
KW - Lipid peroxidation
KW - Nitric oxide
KW - Oxygen radical
UR - http://www.scopus.com/inward/record.url?scp=0032513129&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032513129&partnerID=8YFLogxK
U2 - 10.1016/S0014-5793(98)00173-2
DO - 10.1016/S0014-5793(98)00173-2
M3 - Article
VL - 424
SP - 197
EP - 201
JO - FEBS Letters
T2 - FEBS Letters
JF - FEBS Letters
SN - 0014-5793
IS - 3
ER -