Nicotinamide의 투여가 일시적인 국소허혈로 유발된 흰쥐의 뇌경색에 미치는 영향
Nicotinamide Reduces the Infarct Volume in a Rat Model of Transient Middle Cerebral Artery Occlusion
이민섭, 안영준, 최기용, 강구, 정일영, 김근우, 강성식, 이건재,
소속 상세정보
이민섭 ( Lee Min-Sup )
강원대학교 의과대학 병리학교실
안영준 ( Ahn Young-Jun )
강원대학교 의과대학 병리학교실
최기용 ( Choi Ki-Young )
강원대학교 의과대학 병리학교실
강구 ( Kang Gu )
강원대학교 의과대학 병리학교실
정일영 ( Cheong Il-Young )
강원대학교병원 임상의학연구소
김근우 ( Kim Keun-Woo )
강원대학교병원 임상의학연구소
강성식 ( Kang Seong-Sik )
강원대학교병원 임상의학연구소
이건재 ( Lee Kun-Jai )
강원대학교병원 임상의학연구소
KMID : 0357920060400020093
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.
키워드
Nicotinamide;PARP-1;Nitrotyrosine;Brain ischemia
원문 및 링크아웃 정보
등재저널 정보