Inhibition of NF-kappaB Activation Increases Oxygen-Glucose Deprivation-Induced Cerebral Endothelial Cell Death
The Korean Journal of Physiology and Pharmacology
;
: 65-72, 2003.
Article
in English
| WPRIM
| ID: wpr-727617
ABSTRACT
Increasing evidences suggest that ischemia-induced vascular damage is an integral step in the cascade of the cellular and molecular events initiated by cerebral ischemia. In the present study, employing a mouse brain endothelioma-derived cell line, bEnd.3, and oxygen-glucose deprivation (OGD) as an in vitro stroke model, the role of nuclear factor kappa B (NF-kappaB) activation during ischemic injury was investigated. OGD was found to activate NF-kappaB and to induce bEnd.3 cell death in a time-dependent manner. OGD phosphorylated neither 32 Ser nor 42 Tyr of IkappaBalpha. OGD did not change the amount of IkappaB alpha. The extents of OGD-induced cell death after 8 h, 10 h, 12 h and 14 h of OGD were 10%, 35%, 60% and 85%, respectively. Reperfusion following OGD did not cause additional cell death, indicating no reperfusion injury after ischemic insult in cerebral endothelial cells. Three known as NF-kappaB inhibitors, including pyrrolidine dithiocarbamate (PDTC) plus zinc, aspirin and caffeic acid phenethyl ester (CAPE), inhibited OGD-induced NF-kappaB activation and increased OGD-induced bEnd.3 cell death in a dose dependent manner. There were no changes in the protein levels of bcl-2, bax and p53 which are modulated by NF-kappaB activity. These results suggest that NF-kappaB activation might be a protective mechanism for OGD-induced cell death in bEnd.3.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Zinc
/
Brain
/
Reperfusion
/
Reperfusion Injury
/
Cell Line
/
Brain Ischemia
/
Aspirin
/
NF-kappa B
/
Cell Death
/
Stroke
Type of study:
Prognostic study
Limits:
Animals
Language:
English
Journal:
The Korean Journal of Physiology and Pharmacology
Year:
2003
Type:
Article
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