Protective role of caffeic acid in an Abeta 25-35-induced Alzheimer's disease model
2015
Kim, J.H., Pusan National University, Busan, Republic of Korea | Wang, Q., Pusan National University, Busan, Republic of Korea | Choi, J.M., Pusan National University, Busan, Republic of Korea | Lee, S., Chung-Ang University, Anseong, Republic of Korea | Cho, E.J., Pusan National University, Busan, Republic of Korea
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 Abeta 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 Abeta25-35-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 Abeta25-35-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 Abeta25-35-induced memory deficits and cognitive impairment through inhibition of lipid peroxidation and NO production.
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