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    Neuroprotective Effects of Icariin on Brain Metabolism, Mitochondrial Functions, and Cognition in Triple-Transgenic Alzheimer's Disease Mice.

    Abstract

    AIMS

    This study investigated the neuroprotective properties of icariin (an effective component of traditional Chinese herbal medicine Epimedium) on neuronal function and brain energy metabolism maintenance in a triple-transgenic mouse model of Alzheimer's disease (3 × Tg-AD).

    METHODS

    3 × Tg-AD mice as well as primary neurons were subjected to icariin treatment. Morris water maze assay, magnetic resonance spectroscopy (MRS), Western blotting, ELISA, and immunohistochemistry analysis were used to evaluate the effects of icariin administration.

    RESULTS

    Icariin significantly improved spatial learning and memory retention in 3 × Tg-AD mice, promoted neuronal cell activity as identified by the enhancement of brain metabolite N-acetylaspartate level and ATP production in AD mice, preserved the expressions of mitochondrial key enzymes COX IV, PDHE1α, and synaptic protein PSD95, reduced Aβ plaque deposition in the cortex and hippocampus of AD mice, and inhibited β-site APP cleavage enzyme 1 (BACE1) expression. Icariin treatment also decreased the levels of extracellular and intracellular Aβ1-42 in 3 × Tg-AD primary neurons, modulated the distribution of Aβ along the neurites, and protected against mitochondrial fragmentation in 3 × Tg-AD neurons.

    CONCLUSIONS

    Icariin shows neuroprotective effects in 3 × Tg-AD mice and may be a promising multitarget drug in the prevention/protection against AD.

    Links

  • Publisher Full Text

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    Authors+Show Affiliations

    Chen YJ
    ,

    College of Life Science, Shenzhen Key Laboratory of Marine Bioresources and Ecology, Shenzhen University, Shenzhen, China.

    Zheng HY
    ,

    College of Life Science, Shenzhen Key Laboratory of Marine Bioresources and Ecology, Shenzhen University, Shenzhen, China.

    Huang XX
    ,

    College of Life Science, Shenzhen Key Laboratory of Microbial Genetic Engineering, Shenzhen University, Shenzhen, China.

    Han SX
    ,

    College of Life Science, Shenzhen Key Laboratory of Marine Bioresources and Ecology, Shenzhen University, Shenzhen, China.

    Zhang DS
    ,

    College of Life Science, Shenzhen Key Laboratory of Microbial Genetic Engineering, Shenzhen University, Shenzhen, China.

    Ni JZ
    ,

    College of Life Science, Shenzhen Key Laboratory of Marine Bioresources and Ecology, Shenzhen University, Shenzhen, China.

    He XY

    College of Life Science, Shenzhen Key Laboratory of Marine Bioresources and Ecology, Shenzhen University, Shenzhen, China.

    Source

    CNS neuroscience & therapeutics 22:1 2016 Jan pg 63-73

    MeSH

    Alzheimer Disease
    Amyloid beta-Protein Precursor
    Animals
    Brain
    Cells, Cultured
    Cognition
    Disease Models, Animal
    Drug Evaluation, Preclinical
    Female
    Flavonoids
    Humans
    Maze Learning
    Mice, Transgenic
    Mitochondria
    Neurons
    Neuroprotective Agents
    Presenilin-1
    Spatial Memory
    tau Proteins

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    26584824

    Citation

    Chen, Yi-Jing, et al. "Neuroprotective Effects of Icariin On Brain Metabolism, Mitochondrial Functions, and Cognition in Triple-Transgenic Alzheimer's Disease Mice." CNS Neuroscience & Therapeutics, vol. 22, no. 1, 2016, pp. 63-73.
    Chen YJ, Zheng HY, Huang XX, et al. Neuroprotective Effects of Icariin on Brain Metabolism, Mitochondrial Functions, and Cognition in Triple-Transgenic Alzheimer's Disease Mice. CNS Neurosci Ther. 2016;22(1):63-73.
    Chen, Y. J., Zheng, H. Y., Huang, X. X., Han, S. X., Zhang, D. S., Ni, J. Z., & He, X. Y. (2016). Neuroprotective Effects of Icariin on Brain Metabolism, Mitochondrial Functions, and Cognition in Triple-Transgenic Alzheimer's Disease Mice. CNS Neuroscience & Therapeutics, 22(1), pp. 63-73. doi:10.1111/cns.12473.
    Chen YJ, et al. Neuroprotective Effects of Icariin On Brain Metabolism, Mitochondrial Functions, and Cognition in Triple-Transgenic Alzheimer's Disease Mice. CNS Neurosci Ther. 2016;22(1):63-73. PubMed PMID: 26584824.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Neuroprotective Effects of Icariin on Brain Metabolism, Mitochondrial Functions, and Cognition in Triple-Transgenic Alzheimer's Disease Mice. AU - Chen,Yi-Jing, AU - Zheng,Hai-Yang, AU - Huang,Xiu-Xian, AU - Han,Shuang-Xue, AU - Zhang,Dong-Sheng, AU - Ni,Jia-Zuan, AU - He,Xiao-Yang, Y1 - 2015/11/20/ PY - 2015/03/31/received PY - 2015/09/18/revised PY - 2015/10/04/accepted PY - 2015/11/21/entrez PY - 2015/11/21/pubmed PY - 2016/10/19/medline KW - Alzheimer's disease KW - Icariin KW - Magnetic resonance spectroscopy KW - Mitochondrial dysfunction KW - N-acetylaspartate SP - 63 EP - 73 JF - CNS neuroscience & therapeutics JO - CNS Neurosci Ther VL - 22 IS - 1 N2 - AIMS: This study investigated the neuroprotective properties of icariin (an effective component of traditional Chinese herbal medicine Epimedium) on neuronal function and brain energy metabolism maintenance in a triple-transgenic mouse model of Alzheimer's disease (3 × Tg-AD). METHODS: 3 × Tg-AD mice as well as primary neurons were subjected to icariin treatment. Morris water maze assay, magnetic resonance spectroscopy (MRS), Western blotting, ELISA, and immunohistochemistry analysis were used to evaluate the effects of icariin administration. RESULTS: Icariin significantly improved spatial learning and memory retention in 3 × Tg-AD mice, promoted neuronal cell activity as identified by the enhancement of brain metabolite N-acetylaspartate level and ATP production in AD mice, preserved the expressions of mitochondrial key enzymes COX IV, PDHE1α, and synaptic protein PSD95, reduced Aβ plaque deposition in the cortex and hippocampus of AD mice, and inhibited β-site APP cleavage enzyme 1 (BACE1) expression. Icariin treatment also decreased the levels of extracellular and intracellular Aβ1-42 in 3 × Tg-AD primary neurons, modulated the distribution of Aβ along the neurites, and protected against mitochondrial fragmentation in 3 × Tg-AD neurons. CONCLUSIONS: Icariin shows neuroprotective effects in 3 × Tg-AD mice and may be a promising multitarget drug in the prevention/protection against AD. SN - 1755-5949 UR - https://www.unboundmedicine.com/medline/citation/26584824/Neuroprotective_Effects_of_Icariin_on_Brain_Metabolism_Mitochondrial_Functions_and_Cognition_in_Triple_Transgenic_Alzheimer's_Disease_Mice_ L2 - https://doi.org/10.1111/cns.12473 DB - PRIME DP - Unbound Medicine ER -