Inhibition of NF-κB activation increases oxygen-glucose deprivation-induced cerebral endothelial cell death

Jinu Lee, Chul Hoon Kim, Kyu Dae Shim, Young Soo Ahn

Research output: Contribution to journalArticle

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-κB) activation during ischemic injury was investigated. OGD was found to activate NF-κB and to induce bEnd.3 cell death in a time-dependent manner. OGD phosphorylated neither 32 Ser nor 42 Tyr of I κ B α. OGD did not change the amount of I κ B α. 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-κB inhibitors, including pyrrolidine dithiocarbamate (PDTC) plus zinc, aspirin and caffeic acid phenethyl ester (CAPE), inhibited OGD-induced NF-κB 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-κB activity. These results suggest that NF-κB activation might be a protective mechanism for OGD-induced cell death in bEnd.3.

Original languageEnglish
Pages (from-to)65-71
Number of pages7
JournalKorean Journal of Physiology and Pharmacology
Volume7
Issue number2
Publication statusPublished - 2003 Apr 1

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NF-kappa B
Cell Death
Endothelial Cells
Oxygen
Glucose
Reperfusion Injury
Brain Ischemia
Aspirin
Reperfusion
Blood Vessels
Zinc
Ischemia
Stroke
Cell Line

All Science Journal Classification (ASJC) codes

  • Physiology
  • Pharmacology

Cite this

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title = "Inhibition of NF-κB activation increases oxygen-glucose deprivation-induced cerebral endothelial cell death",
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-κB) activation during ischemic injury was investigated. OGD was found to activate NF-κB and to induce bEnd.3 cell death in a time-dependent manner. OGD phosphorylated neither 32 Ser nor 42 Tyr of I κ B α. OGD did not change the amount of I κ B α. 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-κB inhibitors, including pyrrolidine dithiocarbamate (PDTC) plus zinc, aspirin and caffeic acid phenethyl ester (CAPE), inhibited OGD-induced NF-κB 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-κB activity. These results suggest that NF-κB activation might be a protective mechanism for OGD-induced cell death in bEnd.3.",
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Inhibition of NF-κB activation increases oxygen-glucose deprivation-induced cerebral endothelial cell death. / Lee, Jinu; Kim, Chul Hoon; Shim, Kyu Dae; Ahn, Young Soo.

In: Korean Journal of Physiology and Pharmacology, Vol. 7, No. 2, 01.04.2003, p. 65-71.

Research output: Contribution to journalArticle

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