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http://dx.doi.org/10.4162/nrp.2015.9.5.480

Protective role of caffeic acid in an Aβ25-35-induced Alzheimer's disease model  

Kim, Ji Hyun (Department of Food Science and Nutrition, and Kimchi Research Institute, Pusan National University)
Wang, Qian (Department of Food Science and Nutrition, and Kimchi Research Institute, Pusan National University)
Choi, Ji Myung (Department of Food Science and Nutrition, and Kimchi Research Institute, Pusan National University)
Lee, Sanghyun (Department of Integrative Plant Science, Chung-Ang University)
Cho, Eun Ju (Department of Food Science and Nutrition, and Kimchi Research Institute, Pusan National University)
Publication Information
Nutrition Research and Practice / v.9, no.5, 2015 , pp. 480-488 More about this Journal
Abstract
BACKGROUND/OBJECTIVES: Alzheimer's disease (AD) is characterized by deficits in memory and cognitive functions. The accumulation of amyloid beta peptide ($A{\beta}$) 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 $A{\beta}_{25-35}$-injected AD mouse model. CA was administered at an oral dose of 10 or 50 mg/kg/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 $A{\beta}_{25-35}$-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 $A{\beta}_{25-35}$-injected control group. In particular, CA 50 mg/kg/day showed the stronger protective effect from cognitive impairment than CA 10 mg/kg/day. CONCLUSIONS: The present results suggest that CA improves $A{\beta}_{25-35}$-induced memory deficits and cognitive impairment through inhibition of lipid peroxidation and NO production.
Keywords
Caffeic acid; Alzheimer's disease; amyloid beta; oxidative stress; nitric oxide;
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