β-淀粉样蛋白25-35致伤对PC12神经元突触相关蛋白表达的影响

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

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.