Journal of Pathology and Translational Medicine (대한병리학회지)

The Korean Society of Pathologists (대한병리학회)
권호 표지

Nicotinamide Reduces the Infarct Volume in a Rat Model of Transient Middle Cerebral Artery Occlusion

Nicotinamide의 투여가 일시적인 국소허혈로 유발된 흰쥐의 뇌경색에 미치는 영향

Lee, Min-Sup;Ahn, Young-Jun;Choi, Ki-Young;Kang, Gu;Kang, Seong-Sik;Cheong, Il-Young;Lee, Kun-Jai;Kim, Keun-Woo
이민섭;안영준;최기용;강구;강성식;정일영;이건재;김근우

  • Published : 20060400
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Abstract

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.

Keywords

References

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