지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2015.10
- 수록면
- 480 - 488 (9page)
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초록· 키워드
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BACKGROUND/OBJECTIVES: Alzheimer’s disease (AD) is characterized by deficits in memory and cognitive functions. The accumulation of amyloid beta peptide (Aβ) and oxidative stress in the brain are the most common causes of AD.
MATERIALS/METHODS: Caffeic acid (CA) is an active phenolic compound that has a variety of pharmacological actions. We studied the protective abilities of CA in an Aβ25-35-injected AD mouse model. CA was administered at an oral dose of 10 or 50 ㎎/㎏/day for 2 weeks. Behavioral tests including T-maze, object recognition, and Morris water maze were carried out to assess cognitive abilities. In addition, lipid peroxidation and nitric oxide (NO) production in the brain were measured to investigate the protective effect of CA in oxidative stress.
RESULTS: In the T-maze and object recognition tests, novel route awareness and novel object recognition were improved by oral administration of CA compared with the Aβ25-35-injected control group. These results indicate that administration of CA improved spatial cognitive and memory functions. The Morris water maze test showed that memory function was enhanced by administration of CA. In addition, CA inhibited lipid peroxidation and NO formation in the liver, kidney, and brain compared with the Aβ25-35-injected control group. In particular, CA 50 ㎎/㎏/day showed the stronger protective effect from cognitive impairment than CA 10 ㎎/㎏/day.
CONCLUSIONS: The present results suggest that CA improves Aβ25-35-induced memory deficits and cognitive impairment through inhibition of lipid peroxidation and NO production.
MATERIALS/METHODS: Caffeic acid (CA) is an active phenolic compound that has a variety of pharmacological actions. We studied the protective abilities of CA in an Aβ25-35-injected AD mouse model. CA was administered at an oral dose of 10 or 50 ㎎/㎏/day for 2 weeks. Behavioral tests including T-maze, object recognition, and Morris water maze were carried out to assess cognitive abilities. In addition, lipid peroxidation and nitric oxide (NO) production in the brain were measured to investigate the protective effect of CA in oxidative stress.
RESULTS: In the T-maze and object recognition tests, novel route awareness and novel object recognition were improved by oral administration of CA compared with the Aβ25-35-injected control group. These results indicate that administration of CA improved spatial cognitive and memory functions. The Morris water maze test showed that memory function was enhanced by administration of CA. In addition, CA inhibited lipid peroxidation and NO formation in the liver, kidney, and brain compared with the Aβ25-35-injected control group. In particular, CA 50 ㎎/㎏/day showed the stronger protective effect from cognitive impairment than CA 10 ㎎/㎏/day.
CONCLUSIONS: The present results suggest that CA improves Aβ25-35-induced memory deficits and cognitive impairment through inhibition of lipid peroxidation and NO production.
목차
INTRODUCTION5
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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