Preventive Effect of Caffeine on Alzheimer's Disease
10.13241/j.cnki.pmb.2017.23.011
- VernacularTitle:咖啡因预防阿尔兹海默病作用机制的研究
- Author:
Qianqian HOU
;
Xuejiao CAO
;
Jiabao WANG
;
Wenjing GUO
;
Xudong HOU
;
Cuili ZHANG
- Keywords:
Caffeine;
Aging model;
Brain Derived Neurotrophic Factor (BDNF);
Extracellular signal-regulated kinases1/2(ERK1/2);
Alzheimer's disease
- From:
Progress in Modern Biomedicine
2017;17(23):4452-4455,4571
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the effects of caffeine on the prevention of Alzheimer's disease (AD).Methods:Use Ethanol as a solvent to extract the caffeine in tea and then injecting 5％ D-galactose saline solution 1ml/d/kg to establish aging model mice.Divide mice randomly into experimental group (high-dose/low-dosecaffeine),positive control group,negative control group,and normal con-trol group (NS) and injecting appropriate drugs for consecutive four weeks.Test superoxyde dismutase (SOD) and malondialdehvde (MDA) periodically.Take mice's hippocampus and use Western blotting to detect the expression of brain derived neurotrophic factor (BDNF) and extracellular signal-regulated kinasesl/2 (p-ERK1/2).Results:The expression of BDNF and p-ERK1/2,negative control group is less than low-dose experimental group and positive control group (P＜0.01);The p-ERK1/2 expression of injecting D-galactose mice was significantly lower than normal group,negative control group compared weth the normal group,the differencd was significant (P＜0.05).The level of SOD in model group was significantly lower than that in normal control group,high,low dose caffeine group and positive control group (P＜0.01),but the level of MDA is opposite.Conclusions:Caffeine can delay aging process by increasing the level of SOD in aging mice,and enhancing the expression of BDNF and P-ERK1/2.Caffeine does a lot to prevent AD.
