吴茱萸碱
莫里斯水上航行任务
转基因小鼠
免疫印迹
医学
内科学
药理学
内分泌学
阿尔茨海默病
转基因
化学
海马体
疾病
生物化学
基因
作者
Shumin Yuan,Kai Gao,Dongmei Wang,Xiong-zhi Quan,Jing Wang,Chunmei Ma,Chuan Qin,Lianfeng Zhang
摘要
To investigate the effect of evodiamine (a quinolone alkaloid from the fruit of Evodia rutaecarpa) on the progression of Alzheimer's disease in SAMP8 and APP(swe)/PS1(ΔE9) transgenic mouse models.The mice at age of 5 months were randomized into the model group, two evodiamine (50 mg·kg(-1)·d(-1) and 100 mg·kg(-1)·d(-1)) groups and an Aricept (2 mg·kg(-1)·d(-1)) group. The littermates of no-transgenic mice and senescence accelerated mouse/resistance 1 mice (SAMR1) were used as controls. After 4 weeks of treatment, learning abilities and memory were assessed using Morris water-maze test, and glucose uptake by the brain was detected using positron emission tomography/computed tomography (PET/CT). Expression levels of IL-1β, IL-6, and TNF-α in brain tissues were detected using ELISA. Expression of COX-2 protein was determined using Western blot.In Morris water-maze test, evodiamine (100 mg·kg(-1)·d(-1)) significantly alleviated the impairments of learning ability and memory. Evodiamine (100 mg·kg(-1)·d(-1)) also reversed the inhibition of glucose uptake due to development of Alzheimer's disease traits in mice. Furthermore, the dose of evodiamine significantly decreased the expression of IL-1β, IL-6, TNF-α, and COX-2 that were involved in the inflammation due to Alzheimer's disease.The results indicate that evodiamine (100 mg·kg(-1)·d(-1)) improves cognitive abilities in the transgenic models of Alzheimer's disease.
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