The mitochondria/caspase-dependent apoptotic pathway plays a role in the positive effects of a power frequency electromagnetic field on Alzheimer’s disease neuronal model

Abstract

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.