Biomedical & Molecular Imaging Center, National Taiwan University College of Medicine, Taipei, Taiwan.
Department of Physics, Lab for Medical Physics & Biomedical Engineering, National Taiwan University, Taipei, Taiwan.
Medicine (Baltimore). 2023 Aug 4;102(31):e34460. doi: 10.1097/MD.0000000000034460.
Neurodegenerative diseases (NDDs) pose a significant global health threat. In particular, Alzheimer disease, the most common type causing dementia, remains an incurable disease. Alzheimer disease is thought to be associated with an imbalance of reactive oxygen species (ROS) in neurons, and scientists considered ROS modulation as a promising strategy for novel remedies. In the study, human neural cell line SH-SY5Y was used in probing the effect of combining noninvasive 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) and the downstream pro-survival and antioxidant proteins as the mechanism underlying neuron protection. These findings highlighted the potential of H-LIPEF combined with BDNF in the treatment of NDDs. Furthermore, BDNF-mimetic drugs combining with noninvasive H-LIPEF to patients is a promising approach worthy of further research. This points to strategies for selecting drugs to cooperate with electric fields in treating neurodegenerative disorders.
神经退行性疾病（NDDs）是一个重大的全球健康威胁。特别是阿尔茨海默病，作为导致痴呆的最常见类型，仍然是一种无法治愈的疾病。阿尔茨海默病被认为与神经元中活性氧物种（ROS）的失衡有关，科学家们认为 ROS 调节是一种有前途的新型治疗策略。在这项研究中，采用人神经细胞系 SH-SY5Y 来探究联合使用非侵入性高频低强度脉冲电场（H-LIPEF）和脑源性神经营养因子（BDNF）对过氧化氢（H2O2）诱导的神经元损伤的保护作用。我们的结果发现，联合治疗方法显著增强了神经保护作用，这可能是由于 H-LIPEF 和 BDNF 协同增加了磷酸化表皮生长因子受体（p-EGFR）的表达水平，从而诱导了与生存相关的丝裂原激活蛋白激酶（MAPK）蛋白。研究证实，细胞外信号调节激酶（ERK）的激活及其下游的促生存和抗氧化蛋白是神经元保护的机制。这些发现强调了 H-LIPEF 联合 BDNF 治疗 NDDs 的潜力。此外，BDNF 模拟药物联合非侵入性 H-LIPEF 应用于患者是一种有前途的值得进一步研究的方法。这为选择药物与电场联合治疗神经退行性疾病的策略提供了思路。
