Institute of Neuroscience, Basic Medical College, Kunming Medical University, Kunming, Yunnan 650500, China.
Department of Anatomy, Changsha Medical University, Changsha, Hunan 410219, China.
Neural Plast. 2022 Nov 10;2022:3995227. doi: 10.1155/2022/3995227. eCollection 2022.
Voltage-gated sodium channel beta 2 (Nav2.2 or Nav2, coded by SCN2B mRNA), a gene involved in maintaining normal physiological functions of the prefrontal cortex and hippocampus, might be associated with prefrontal cortex aging and memory decline. This study investigated the effects of Nav2 in amyloid- 1-42- (A1-42-) induced neural injury model and the potential underlying molecular mechanism. The results showed that Nav2 knockdown restored neuronal viability of A1-42-induced injury in neurons; increased the contents of brain-derived neurotrophic factor (BDNF), enzyme neprilysin (NEP) protein, and NEP enzyme activity; and effectively altered the proportions of the amyloid precursor protein (APP) metabolites including A42, sAPP, and sAPP, thus ameliorating cognitive dysfunction. This may be achieved through regulating NEP transcription and APP metabolism, accelerating A degradation, alleviating neuronal impairment, and regulating BDNF-related signal pathways to repair neuronal synaptic efficiency. This study provides novel evidence indicating that Nav2 plays crucial roles in the repair of neuronal injury induced by A1-42 both and .
电压门控钠离子通道β2（Nav2.2 或 Nav2，由 SCN2B mRNA 编码），参与维持前额叶皮层和海马体的正常生理功能，可能与前额叶皮层衰老和记忆下降有关。本研究探讨了 Nav2 在淀粉样蛋白 1-42-（A1-42-）诱导的神经损伤模型中的作用及其潜在的分子机制。结果表明，Nav2 敲低可恢复 A1-42 诱导的神经元损伤中的神经元活力；增加脑源性神经营养因子（BDNF）、酶神经肽酶（NEP）蛋白和 NEP 酶活性的含量；并有效改变淀粉样前体蛋白（APP）代谢物包括 A42、sAPP 和 sAPP 的比例，从而改善认知功能障碍。这可能是通过调节 NEP 转录和 APP 代谢，加速 A 降解，减轻神经元损伤，以及调节 BDNF 相关信号通路来修复神经元突触效率来实现的。本研究提供了新的证据，表明 Nav2 在 A1-42 诱导的神经元损伤修复中发挥着关键作用。
