TY - JOUR
T1 - Nicotinamide reduces infarction up to two hours after the onset of permanent focal cerebral ischemia in Wistar rats
AU - Ayoub, Issam A.
AU - Jian Lee, E.
AU - Ogilvy, Christopher S.
AU - Flint Beal, M.
AU - Maynard, Kenneth I.
N1 - Funding Information:
The authors thank Dr. Adelbert Ames III and Dr. Eng H. Lo for constructive comments on the manuscript. K.I.M. is an American Heart Association Minority Scientist Development Awardee; C.S.O. is supported by NIH grant #NS01732, and M.F.B. is supported by NIH grants #NS32365 and #NS31579.
PY - 1999/1/4
Y1 - 1999/1/4
N2 - 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.
AB - 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.
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U2 - 10.1016/S0304-3940(98)00881-7
DO - 10.1016/S0304-3940(98)00881-7
M3 - Article
C2 - 10027546
AN - SCOPUS:0345129985
SN - 0304-3940
VL - 259
SP - 21
EP - 24
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 1
ER -