The protective mechanism underlying phenylethanoid glycosides (PHG) actions on synaptic plasticity in rat Alzheimer's disease model induced by beta amyloid 1-42

Autor: Jian-Xin Jia, He Wang, Wei Song, Xu-Sheng Yan, Dong-Sheng Huo, Zhi-Ping Cai, Zhan-Jun Yang, Fang Xin
Rok vydání: 2018
Předmět:
0301 basic medicine
Male
medicine.medical_specialty
Cistanche
Amyloid
Health
Toxicology and Mutagenesis
Tau protein
Nerve Tissue Proteins
tau Proteins
Hippocampal formation
Toxicology
Protective Agents
Receptors
N-Methyl-D-Aspartate
Superoxide dismutase
03 medical and health sciences
Random Allocation
0302 clinical medicine
Western blot
Alzheimer Disease
Internal medicine
medicine
Animals
Cognitive Dysfunction
Glycosides
Phosphorylation
Rats
Wistar
CA1 Region
Hippocampal
chemistry.chemical_classification
Amyloid beta-Peptides
Neuronal Plasticity
biology
medicine.diagnostic_test
Glutathione peroxidase
Pyramidal Cells
Post-Synaptic Density
Rats
030104 developmental biology
Endocrinology
Infusions
Intraventricular
chemistry
Synaptic plasticity
biology.protein
Postsynaptic density
030217 neurology & neurosurgery
Zdroj: Journal of toxicology and environmental health. Part A. 81(21)
ISSN: 1528-7394
Popis: Phenylethanoid glycosides (PHG), derived from Herba cistanche, were found to exert protective effects on cognitive dysfunctions by improving synaptic plasticity in Alzheimer's disease (AD) rat model. However, the mechanisms underlying these effects of PHG on synaptic plasticity remain to be determined. Thus the aim of this study was to examine the influence of PHG on synaptic plasticity in male AD rat model induced by bilateral central nervous system ventricle injections of beta amyloid 1-42 oligomers (Aβ1-42). The following parameters were measured: (1) number of intact pyramidal cells in hippocampal CA1 region by Nissl staining, (2) post synaptic density 95 (PSD-95), phosphorylated N-methyl-D-aspartate receptor-1(p-NMDAR1) and (3) phosphorylated Tau protein (p-Tau) by immunohistochemistry and western blot. In addition, the content of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were determined. Aβ1-42 lowered the number of intact pyramidal cells in hippocampal CA1 region. In contrast, treatment with PHG significantly elevated this cell number. Aβ1-42 significantly diminished protein expression levels of PSD-95 accompanied by elevated protein expression levels of p-NMDAR1 and p-Tau. PHG markedly increased protein expression levels of PSD-95, but significantly reduced protein expression levels of p-NMDAR1 and p-Tau. Further, Aβ1-42 markedly increased MDA content concomitantly with reduced activities of SOD and GSH-Px. PHG significantly decreased MDA content accompanied by elevated activities of SOD and GSH-Px. Data suggest that the protective effects of PHG on synaptic plasticity may involve inhibition of cytotoxicity-mediated by Aβ-1-42 administration and reduction of oxidant stress.
Databáze: OpenAIRE
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