Nicotinamide reduces infarction up to two hours after the onset of permanent focal cerebral ischemia in Wistar rats

Issam A. Ayoub, E. Jian Lee, Christopher S. Ogilvy, M. Flint Beal, Kenneth I. Maynard

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101 Citations (Scopus)

Abstract

Ischemia depletes ATP and initiates cascades leading to irreversible tissue injury. Nicotinamide is a precursor of nicotinamide adenine dinucleotide (NAD+) which increases neuronal ATP concentration and protects against malonate-induced neurotoxicity, trauma and nitric oxide toxicity. We therefore examined whether nicotinamide could protect against stroke, using a model of permanent middle cerebral artery occlusion (MCA) occlusion in Wistar rats. Nicotinamide reduced neuronal infarction in a dose-specific manner. Furthermore, nicotinamide (500 mg/kg) reduced infarcts when administered up to 2 h after the onset of permanent MCA occlusion. The mechanism of action underlying the neuroprotection observed with nicotinamide remains to be clarified. These results are potentially important since nicotinamide is already used clinically, though not in the treatment of stroke.

Original languageEnglish
Pages (from-to)21-24
Number of pages4
JournalNeuroscience Letters
Volume259
Issue number1
DOIs
Publication statusPublished - 1999 Jan 4

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

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