Albiflorin ameliorates memory deficits in APP/PS1 transgenic mice via ameliorating mitochondrial dysfunction
Autor: | Yu Mei, Li Guan, Yi-Jun Xu, Xin-Yue Wang, Qi Wang, Yi-Fang Zhang, Xue-Qing Shi, Huafeng Pan |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Genetically modified mouse Bridged-Ring Compounds Male Synapsin I MFN2 Hippocampus Mice Transgenic Pharmacology 03 medical and health sciences Amyloid beta-Protein Precursor Mice 0302 clinical medicine Alzheimer Disease Memory mental disorders Presenilin-1 MFN1 Animals Molecular Biology chemistry.chemical_classification Neurons Reactive oxygen species Memory Disorders Amyloid beta-Peptides biology Chemistry General Neuroscience Brain Mitochondria Mice Inbred C57BL Disease Models Animal 030104 developmental biology nervous system Apoptosis Synaptophysin biology.protein Neurology (clinical) 030217 neurology & neurosurgery Developmental Biology |
Zdroj: | Brain research. 1719 |
ISSN: | 1872-6240 |
Popis: | Albiflorin, the main component of Radix Paeoniae Alba, has been shown to ameliorate injury in cell models of Alzheimer’s disease induced by amyloid-β (Aβ), but the mechanism is unclear. We used 7-month-old APP/PS1 mice to determine whether albiflorin is capable of protecting against Alzheimer’s disease. We found that four weeks of intragastric administration of albiflorin (20 mg/kg/d and 40 mg/kg/d) ameliorated memory deficits in APP/PS1 mice. Albiflorin conferred synaptic protection by decreasing Aβ levels and increasing PSD-95, synaptophysin and synapsin 1 levels in the brains of APP/PS1 mice. Albiflorin played an antioxidative role by reducing reactive oxygen species (ROS) levels and elevating Mn-SOD activity in the brain. Albiflorin also reduced the level of Drp1, increased the levels of Mfn1, Mfn2 and Opa1 and improved mitochondrial morphology in APP/PS1 mice. Albiflorin inhibited the mitochondrial pathway of apoptosis by increasing the levels of Bcl-2 and Bcl-xl and decreasing the levels of Bax, caspase-3 and cytochrome c in both the hippocampus and the cortex and by reducing the number of apoptotic cells in the anterior parietal cortex of the APP/PS1 mice. In conclusion, treatment with albiflorin improved mitochondrial function, reduced Aβ deposition in the brain and ameliorated memory deficits in APP/PS1 mice. These findings indicate that albiflorin may serve as a potential antidementia drug. |
Databáze: | OpenAIRE |
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