Effects of amyloid-beta 25-35 on expression of synapse-associated proteins in PC12 neurons

doi:10.3969/j.issn.2095-4344.2016.02.013

Chinese Journal of Tissue Engineering Research ›› 2016, Vol. 20 ›› Issue (2): 224-229.doi: 10.3969/j.issn.2095-4344.2016.02.013

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Effects of amyloid-beta 25-35 on expression of synapse-associated proteins in PC12 neurons

Zhang Shuang¹, Huang Xin-yan², Liu Shuang³, Li Yan-jun³, Zhao Jin-cheng³

¹College of Pharmacy, Jiamusi University, Jiamusi 154007, Heilongjiang Province, China; ²Second Affiliated Hospital of Jiamusi University, Jiamusi 154007, Heilongjiang Province, China; ³Basic Medical College, Jiamusi University, Jiamusi 154007, Heilongjiang Province, China

Online:2016-01-08 Published:2016-01-08
Contact: Zhao Jin-cheng, Professor, Basic Medical College of Jiamusi University, Jiamusi 154007, Heilongjiang Province, China
About author:Zhang Shuang, Studying for master’s degree, College of Pharmacy, Jiamusi University, Jiamusi 154007, Heilongjiang Province, China
Supported by:
the Scientific Research Project of Heilongjiang Educational Department, No. 1251666; the Basic Research Project of Jiamusi University, No. 12Z1201502; the Graduate Scientific Innovation Project of Jiamusi University, No. LZZ2014_030

Abstract

Abstract:

BACKGROUND: An amyloid-beta (Aβ) aggregation in the brain can induce nerve cell apoptosis, loss of synapses and functional damage. However, there is still no effective intervention. Improving the synaptic plasticity provides an important direction for the treatment of early Alzheimer’s disease.
OBJECTIVE: To screen the best model of Alzheimer’s disease and to explore the expression of synapse-associated proteins in Aβ25-35-injured PC12 neurons.
METHODS: PC12 cells were induced by 50 μg/L nerve growth factor to differentiate into neuronal-like cells. Then, these cells were treated with Aβ25-35 at different concentrations. Consequently, cell survival rate was detected using cell counting kit-8; neurogranin and neuregulin immunofluorescence stainings were used to observe morphological changes of model cells; western blot used to detect the expression level of neurogranin, calmodulin kinase II, postsynaptic density-95 proteins.
RESULTS AND CONCLUSION: Over time, the survival rate of PC12 neurons induced by Aβ25-35 was decreased in a dose-dependent manner. Shortened synaptic length, neuronal atrophy and sparsely interconnected neurons were visible. Expression levels of neurogranin, calmodulin kinase II and postsynaptic density-95 proteins were all down-regulated. These findings indicate that to screen the cell model of Alzheimer’s disease, the optimal concentration and interventional time of Aβ25-35 are 10 μmol/L and 48 hours, respectively.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

Zhang Shuang, Huang Xin-yan, Liu Shuang, Li Yan-jun, Zhao Jin-cheng . Effects of amyloid-beta 25-35 on expression of synapse-associated proteins in PC12 neurons[J]. Chinese Journal of Tissue Engineering Research, 2016, 20(2): 224-229.

Figures/Tables 3

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Effects of amyloid-beta 25-35 on expression of synapse-associated proteins in PC12 neurons

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