Protection of high-frequency low-intensity pulsed electric fields and brain-derived neurotrophic factor for SH-SY5Y cells against hydrogen peroxide-induced cell damage

Neurodegenerative diseases have been a major threat to public health worldwide nowadays. In particular, Alzheimer’s disease is the most common type causing dementia which has remained an incurable disease, despite improvement of the symptoms via some therapies. The pathogenic mechanism of Alzheimer’s disease is deemed to be related to the aggregation of beta-amyloid peptide (Aβ), a major cause for amyloid plaques, resulting in neuronal death via the generation of reactive oxygen species (ROS). Scientists have regarded oxidative stress as a potential treatment target in the development of novel remedies. In the study, human neural cell line SH-SY5Y was used in probing the effect of combining non-invasive high-frequency low-intensity pulsed electric field (H-LIPEF) and brain-derived neurotrophic factor (BDNF) in protection against hydrogen peroxide (H2O2)-induced neuron damage. Our result finds that the combination approach has intensified the neuroprotective effect significantly, perhaps due to H-LIPEF and BDNF synergistically increasing the expression level of the phosphorylated epidermal growth factor receptor (p-EGFR), which induces the survival-related mitogen-activated protein kinases (MAPK) proteins. The study confirmed the activation of extracellular signal-regulated kinase (ERK), a member of MAPK family, and the downstream pro-survival and antioxidant proteins as the mechanism underlying neuron protection. These findings have highlighted the potential of H-LIPEF combining with BDNF in the treatment of neurodegenerative diseases. Furthermore, the application of BDNF-mimetic drugs and non-invasive H-LIPEF to patients is a promising approach worthy of further research, and this points to strategies and mechanisms for selecting drugs or compounds to cooperate with electric fields in the treatment of neurodegenerative disorders. ### Competing Interest Statement The authors have declared no competing interest.