A dual role of the NF-kappaB pathway in neonatal hypoxic-ischemic brain damage

Stroke; a Journal of Cerebral Circulation
Cora H NijboerAnnemieke Kavelaars

Abstract

NF-kappaB is a transcription factor that regulates inflammatory and apoptotic pathways. We described previously that intraperitoneal administration of the NF-kappaB inhibitor TAT-NBD at 0 and 3 hours after neonatal hypoxia-ischemia (HI) markedly reduced brain damage. We hypothesize that timing and duration of NF-kappaB inhibition will be a major factor in determining outcome. HI was induced in P7 rats by unilateral carotid artery occlusion and hypoxia. In vivo TAT-NBD effects were determined on cerebral damage, NF-kappaB activity, cytokine expression, and pro- and antiapoptotic molecules. In vitro effects of TAT-NBD were determined using primary neurons and cell lines. HI induced 2 peaks of cerebral NF-kappaB activity at 3 to 6 and 24 hours after HI. Neuroprotective 0/3-hour TAT-NBD treatment only inhibited early NF-kappaB activity. However, inhibition of both early and late NF-kappaB-activity by 0/6/12-hour TAT-NBD or only late NF-kappaB activity by 18/21-hour TAT-NBD aggravated damage. 0/6/12-hour TAT-NBD did not prevent HI-induced upregulation of cytokines at 24 hours after HI. Protective 0/3-hour TAT-NBD treatment prevented nuclear accumulation of p53 at 24 hours after HI. Nuclear p53 was not reduced after 0/6/12-hour TAT-N...Continue Reading

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