In this study, rat pheochromocytoma (PC12) cells were induced into an Alzheimer's Disease (AD) neuronal model using nerve growth factor (NGF; 50 ng/mL) and Amyloid β25-35 (20 μmol/L). Changes in the morphological structure, cell viability, apoptosis rate, and expression of apoptosis-related protein induced by exposure to a power frequency electromagnetic field (PF-MF; 50 Hz, 100 μT, 24 h) were detected respectively by light and electron microscopy, the MTT assay, immunohistochemistry, flow cytometry and enzyme-linked immunosorbent assays. The results showed that 3-12 h after PF-MF exposure, the pathological injury was improved partly; metabolic activity was promoted and cell apoptosis was inhibited in the AD neuronal model. In addition, PF-MF exposure significantly inhibited the expression of Caspase8, Caspase3, and CytC, but increased the Bcl-2/Bax ratio of the AD neuronal model. Meanwhile, PF-MF seemed to have no effect on the expression of Fas and TNFR1. This study indicated that the mitochondria/caspase-dependent apoptotic pathway plays an important role in the positive effects of PF-MF on an AD neuronal model. The results suggested that PF-MF exposure might have potential therapeutic value for AD, and the underling molecular mechanisms still need further studies.
Keywords: Alzheimer’s disease; Apoptosis; PC12 cells; PF-MF.
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