AIM: 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. METHODS: 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. RESULTS: 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. CONCLUSION: The results indicate that evodiamine (100 mg·kg(-1)·d(-1)) improves cognitive abilities in the transgenic models of Alzheimer's disease.
AIM: 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. METHODS: 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. RESULTS: 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. CONCLUSION: The results indicate that evodiamine (100 mg·kg(-1)·d(-1)) improves cognitive abilities in the transgenic models of Alzheimer's disease.
Authors: Thierry Bussière; Frédérique Bard; Robin Barbour; Henry Grajeda; Terry Guido; Karen Khan; Dale Schenk; Dora Games; Peter Seubert; Manuel Buttini Journal: Am J Pathol Date: 2004-09 Impact factor: 4.307