摘要
目的:探究咖啡因对阿尔茨海默病(AD)的预防作用。方法:乙醇提取茶叶中咖啡因;颈部皮下注射5%D-半乳糖生理盐水溶液,建立小鼠衰老模型;随机分为实验组(高、低剂量咖啡因)、阳性对照组、阴性对照组;另设正常对照组,连续给药4周。检测超氧化物歧化酶(SOD)以及丙二醛(MDA)的水平,取鼠脑海马组织以western blotting检测脑源性神经营养因子(BDNF)和胞外信号调节激酶(p-ERK1/2)表达量,同时制作病理切片,行HE染色。结果:Western blot检测脑海马组织BDNF和p-ERK1/2的表达,阴性对照组的BDNF表达水平明显低于正常组、低剂量组和阳性对照组(P<0.01);注射D-半乳糖的各组小鼠p-ERK1/2的表达明显低于正常组,阴性对照组与正常组比较,差异显著(P<0.05)。模型组SOD活力明显低于正常对照组、高、低剂量咖啡因组和阳性对照组(P<0.01),但MDA含量则相反。结论:咖啡因能提高衰老模型小鼠SOD活力,促进BDNF和p-ERK1/2的表达,延缓衰老进程,对阿尔茨海默病(AD)有预防作用。
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 lml/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.
出处
《现代生物医学进展》
CAS
2017年第23期4452-4455,4571,共5页
Progress in Modern Biomedicine
基金
2014年辽宁省大学生创新创业训练计划项目(201410161000007)
