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The Korean Journal of Pathology 2006;40(2): 93-102.
Nicotinamide Reduces the Infarct Volume in a Rat Model of Transient Middle Cerebral Artery Occlusion.
Min Sup Lee, Young Jun Ahn, Ki Young Choi, Gu Kang, Seong Sik Kang, Il Young Cheong, Kun Jai Lee, Keun Woo Kim
1Department of Pathology, Kangwon National University College of Medicine, Chunchon, Korea. guk@kangwon.ac.kr
2Kangwon National University Hospital Clinical Research Institute, Chunchon, Korea.
BACKGROUND: Cerebral ischemia depletes ATP and causes irreversible tissue injury. Nicotinamide is a precursor of NAD+ and it is also a poly (ADP-ribose) polymerase (PARP) inhibitor that increases the neuronal ATP concentration and so protects against stroke. Therefore we examined whether nicotinamide could protect against cerebral ischemia by using a model of transient middle cerebral artery occlusion (MCAO) (reperfusion 2 h post ischemia) in Sprague-Dawley rats. METHODS: Nicotinamide (500 mg/kg) or normal saline was administered intraperitoneally 24 and 0 h before and after MCAO, respectively. The infarction volumes were determined with triphenyltetrazolium chloride staining 24 h after reperfusion. The nitrotyrosine, PAR polymer and PARP-1 expressions were examined by immunohistochemistry with using brain slices obtained from the rats that were sacrificed at 0, 15, 30, 60 and 120 min after reperfusion. RESULTS: The infarction volumes were significantly attenuated (21.8%, p<0.05). The nitrotyrosine expressions were increased at 0, 15 and 30 min, and those expressions for PARP polymer and PARP-1 were increased at 60 and 120 min, respectively. Nicotinamide partly reduced the expressions for nitrotyrosine and PAR polymer except for PARP-1. CONCLUSIONS: These results suggest that nicotinamide may attenuate ischemic brain injury through its antioxidant activity and the inhibition of PARP-1.
Key Words: Nicotinamide; PARP-1; Nitrotyrosine; Brain ischemia
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