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Article

Pharmacological Basis for the Use of Evodiamine in Alzheimer’s Disease: Antioxidation and Antiapoptosis

1
School of Life Sciences, Jilin University, Changchun 130012, China
2
Department of Pharmacology, College of Basic Medical Sciences, Jilin University, Changchun 130006, China
3
Changchun Shengjinnuo Biological Pharmaceutical Co., Ltd., Changchun 130000, China
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2018, 19(5), 1527; https://doi.org/10.3390/ijms19051527
Received: 7 May 2018 / Revised: 16 May 2018 / Accepted: 16 May 2018 / Published: 21 May 2018
(This article belongs to the Special Issue Neuron Cell Death)
Evodiamine (Evo), a major alkaloid compound isolated from the dry unripened fruit of Evodia fructus, has a wide range of pharmacological activities. The present study sought to explore the neuroprotective effects of Evo in l-glutamate (l-Glu)-induced apoptosis of HT22 cells, and in a d-galactose and aluminum trichloride-developed Alzheimer’s disease (AD) mouse model. Evo significantly enhanced cell viability, inhibited the accumulation of reactive oxygen species, ameliorated mitochondrial function, increased the B-cell lymphoma-2 protein content, and inhibited the high expression levels of Bax, Bad, and cleaved-caspase-3 and -8 in l-Glu-induced HT22 cells. Evo also enhanced the phosphorylation activities of protein kinase B and the mammalian target of rapamycin in the l-Glu-induced HT22 cells. In the AD mouse model, Evo reduced the aimless and chaotic movements, reduced the time spent in the central area in the open field test, and decreased the escape latency time in the Morris water maze test. Evo reduced the deposition of amyloid beta 42 (Aβ42) in the brain, and increased the serum level of Aβ42, but showed no significant effects on Aβ40. In addition, six weeks of Evo administration significantly suppressed oxidative stress by modulating the related enzyme levels. In the central cholinergic system of AD mice, Evo significantly increased the serum levels of acetylcholine and choline acetyltransferase and decreased the level of acetylcholinesterase in the serum, hypothalamus, and brain. Our results provide experimental evidence that Evo can serve as a neuroprotective candidate for the prevention and/or treatment of neurodegenerative diseases. View Full-Text
Keywords: Evodiamine; Alzheimer’s disease; apoptosis; oxidative stress; cholinergic system Evodiamine; Alzheimer’s disease; apoptosis; oxidative stress; cholinergic system
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MDPI and ACS Style

Zhang, Y.; Wang, J.; Wang, C.; Li, Z.; Liu, X.; Zhang, J.; Lu, J.; Wang, D. Pharmacological Basis for the Use of Evodiamine in Alzheimer’s Disease: Antioxidation and Antiapoptosis. Int. J. Mol. Sci. 2018, 19, 1527. https://doi.org/10.3390/ijms19051527

AMA Style

Zhang Y, Wang J, Wang C, Li Z, Liu X, Zhang J, Lu J, Wang D. Pharmacological Basis for the Use of Evodiamine in Alzheimer’s Disease: Antioxidation and Antiapoptosis. International Journal of Molecular Sciences. 2018; 19(5):1527. https://doi.org/10.3390/ijms19051527

Chicago/Turabian Style

Zhang, Yongfeng, Jiaqi Wang, Chunyue Wang, Zhiping Li, Xin Liu, Jun Zhang, Jiahui Lu, and Di Wang. 2018. "Pharmacological Basis for the Use of Evodiamine in Alzheimer’s Disease: Antioxidation and Antiapoptosis" International Journal of Molecular Sciences 19, no. 5: 1527. https://doi.org/10.3390/ijms19051527

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