Xanthoceras sorbifolia extracts ameliorate dendritic spine deficiency and cognitive decline via upregulation of BDNF expression in a rat model of Alzheimer's disease

Autor: Shijie Song, Da-Li Meng, Peng Liu, Xuefei Ji, Lili Wang, Ge Jin, Tianyan Chi, Shimeng Qiu, Libo Zou, Pu Xu, Yinjie Li, Jikai Xu, Yapeng Hou, Chen Zheng
Rok vydání: 2016
Předmět:
0301 basic medicine
Male
rho GTP-Binding Proteins
RHOA
Dendritic spine
Dendritic Spines
Anti-Inflammatory Agents
Hippocampus
Morris water navigation task
Tropomyosin receptor kinase B
Rats
Sprague-Dawley
03 medical and health sciences
0302 clinical medicine
Sapindaceae
Alzheimer Disease
medicine
Animals
Receptor
trkB
Cognitive Dysfunction
Cognitive decline
Brain-derived neurotrophic factor
rho-Associated Kinases
Amyloid beta-Peptides
biology
Behavior
Animal
Plant Extracts
General Neuroscience
Brain-Derived Neurotrophic Factor
Intracellular Signaling Peptides and Proteins
Membrane Proteins
Protein-Tyrosine Kinases
medicine.disease
Peptide Fragments
Rats
Up-Regulation
Disease Models
Animal
030104 developmental biology
nervous system
biology.protein
Alzheimer's disease
Neuroscience
Disks Large Homolog 4 Protein
030217 neurology & neurosurgery
Zdroj: Neuroscience letters. 629
ISSN: 1872-7972
Popis: Xanthoceras sorbifolia, a traditional Chinese folk medicine with anti-inflammatory effects, has been used for a long time in China, especially in the Inner Mongolian area for the treatment of rheumatism. Inflammation is one of the main causes of Alzheimer's disease (AD). AD is characterized by aggregation of amyloid β-peptide (Aβ) plaques, neurofibrillary tangle formation, synaptic dysfunction and neuronal loss. To investigate whether Xanthoceras sorbifolia extracts (XSE) improve cognition and protect dendritic spines, we performed behavioral tests to investigate learning and memory in an Aβ25-35-induced dementia animal model of AD as well as Golgi staining to observe dendritic spine formation in CA1 pyramidal neurons and western blots to test the expression levels of PSD95, BDNF and downstream signaling pathways. Our results indicated that oral treatment with XSE significantly reduced cognitive impairments in behavioral tests (passive avoidance test, novel object recognition test, Y-maze test and Morris water maze test). Golgi staining results revealed that XSE ameliorated dendritic spine density deficits in CA1 pyramidal neurons in the hippocampus. Western blot analysis suggested that XSE upregulated PSD95, which is the major scaffolding protein in synapses. BDNF levels and the ratio of p-TrkB/TrkB increased, and the expression of the RhoA, a member of the Rho-GTPase family, and its downstream target protein ROCK2 decreased in the dementia animal model following treatment with XSE. Therefore, the cognition-improving effects of XSE probably resulted from dendritic spine protection effects through regulation of BDNF signaling pathways.
Databáze: OpenAIRE
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