PDF(Pubmed)
Abstract：
Mitochondria-derived reactive oxygen species production at a moderate physiological level plays a fundamental role in the anti-aging signaling, due to their action as redox-active sensors for the maintenance of optimal mitochondrial balance between intracellular energy status and hormetic nutrients. Iron regulatory protein dysregulation, systematically increased iron levels, mitochondrial dysfunction, and the consequent oxidative stress are recognized to underlie the pathogenesis of multiple neurodegenerative diseases, such as Parkinson\'s disease and Alzheimer\'s disease. Central to their pathogenesis, Nrf2 signaling dysfunction occurs with disruption of metabolic homeostasis. We highlight the potential therapeutic importance of nutritional polyphenols as substantive regulators of the Nrf2 pathway. Here, we discuss the common mechanisms targeting the Nrf2/vitagene pathway, as novel therapeutic strategies to minimize consequences of oxidative stress and neuroinflammation, generally associated to cognitive dysfunction, and demonstrate its key neuroprotective and anti-neuroinflammatory properties, summarizing pharmacotherapeutic aspects relevant to brain pathophysiology.
摘要：
线粒体衍生的活性氧在中等生理水平的产生在抗衰老信号中起着基本作用，由于它们作为氧化还原活性传感器的作用，用于维持细胞内能量状态和营养之间的最佳线粒体平衡。铁调节蛋白失调,系统地增加铁水平，线粒体功能障碍，而随之而来的氧化应激被认为是多种神经退行性疾病发病的基础，如帕金森病和阿尔茨海默病。其发病机制的核心，Nrf2信号传导功能障碍随着代谢稳态的破坏而发生。我们强调了营养多酚作为Nrf2途径的实质性调节剂的潜在治疗重要性。这里,我们讨论了靶向Nrf2/vitagene途径的常见机制，作为新的治疗策略，以尽量减少氧化应激和神经炎症的后果，通常与认知功能障碍有关，并证明其关键的神经保护和抗神经炎症特性，总结与脑部病理生理学相关的药物治疗方面。
