대한한방내과학회지 (The Journal of Internal Korean Medicine)
- 제24권1호
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- Pages.104-112
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- 2003
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- 1226-9174(pISSN)
소합향원(蘇合香元)이 저산소증 유발 배양 대뇌신경세포에 미치는 영향
The Effect of Sohaphyang-won's for Delayed Neuronal Death in Hypoxia
- 윤경선 (동국대학교 한의과대학 내과학교실) ;
- 정승현 (동국대학교 한의과대학 내과학교실) ;
- 신길조 (동국대학교 한의과대학 내과학교실) ;
- 이원철 (동국대학교 한의과대학 내과학교실) ;
- 문일수 (동국대학교 해부학교실) ;
- 이지훈 (동국대학교 한의과대학 내과학교실)
- Yun Kyoung-Sun (Department of Internal Medicine, College of Oriental Medicine, Dongguk University) ;
- Jeong Sung-Hyun (Department of Internal Medicine, College of Oriental Medicine, Dongguk University) ;
- Shin Gil-Cho (Department of Internal Medicine, College of Oriental Medicine, Dongguk University) ;
- Lee Won-Chu (Department of Internal Medicine, College of Oriental Medicine, Dongguk University) ;
- Moon Il-Su (Department of Anatomy, College of Medicine, Dongguk University*) ;
- Lee Ji-Hun (Department of Internal Medicine, College of Oriental Medicine, Dongguk University)
- 발행 : 2003.03.01
초록
Objectives : The purpose of this study is to evaluate the effects of Sohaphyang-won and is to study the mechanism for neuronal death protection in hypoxia with Embryonic day 20(E20) cortical cells of a guinea pig(Sprague Dawley). Methods : E20 cortical cells, used in this investigation were dissociated in Neurobasal media and grown for 14 days in vitro (DIV). On 14 DIV, Sohaphyang-won was added to the culture media for 72 hours. On 17 DIV, cells were given a hypoxic shock and further incubated in normoxia for another three days. On 20 DIV, Sohaphyang-won's effects for neuronal death protection were evaluated by LDH assay and the mechanism was studied by Bcl-2, Bak, Bax, caspase family. Results : This study indicates that Sohaphyang-won's effects for neuronal death protection in hypoxia is confirmed by LDH assay by the method of Embryonic day 20(E20) cortical neuroblast. Conclusions : Sohaphyang-won's mechanism for neuronal death protection in hypoxia restrains inflow of cytochrome C into cellularity caused by Bcl-2 increase and reduces the caspase cascade initiator caspase-10 and the effector caspase-3.