Department of Biological Sciences, University of Alabama, 2320 Science and Engineering Complex, Tuscaloosa, AL 35487-0344, USA.
Department of Biological Sciences, University of Alabama, 2320 Science and Engineering Complex, Tuscaloosa, AL 35487-0344, USA; College of Pharmacy, Department of Pharmaceutical Sciences, University of Illinois at Chicago, Chicago, IL 60612, USA.
Neurotoxicology. 2023 May;96:1-12. doi: 10.1016/j.neuro.2023.02.008. Epub 2023 Feb 21.
Nature-derived bioactive compounds have emerged as promising candidates for the prevention and treatment of diverse chronic illnesses, including neurodegenerative diseases. However, the exact molecular mechanisms underlying their neuroprotective effects remain unclear. Most studies focus solely on the antioxidant activities of natural products which translate to poor outcome in clinical trials. Current therapies against neurodegeneration only provide symptomatic relief, thereby underscoring the need for novel strategies to combat disease onset and progression. We have employed an environmental toxin-induced Drosophila Parkinson's disease (PD) model as an inexpensive in vivo screening platform to explore the neuroprotective potential of selected dietary flavonoids. We have identified a specific group of flavonoids known as flavones displaying protection against paraquat (PQ)-induced neurodegenerative phenotypes involving reduced survival, mobility defects, and enhanced oxidative stress. Interestingly, the other groups of investigated flavonoids, namely, the flavonones and flavonols failed to provide protection indicating a requirement of specific structural features that confer protection against PQ-mediated neurotoxicity in Drosophila. Based on our screen, the neuroprotective flavones lack a functional group substitution at the C3 and contain α,β-unsaturated carbonyl group. Furthermore, flavones-mediated neuroprotection is not solely dependent on antioxidant properties through nuclear factor erythroid 2-related factor 2 (Nrf2) but also requires regulation of the immune deficiency (IMD) pathway involving NFκB and the negative regulator poor Imd response upon knock-in (Pirk). Our data have identified specific structural features of selected flavonoids that provide neuroprotection against environmental toxin-induced PD pathogenesis that can be explored for novel therapeutic interventions.
天然生物活性化合物已成为预防和治疗多种慢性疾病(包括神经退行性疾病)的有前途的候选药物。然而,其神经保护作用的确切分子机制尚不清楚。大多数研究仅关注天然产物的抗氧化活性,这导致临床试验结果不佳。目前针对神经退行性变的治疗方法仅提供症状缓解,因此需要新的策略来对抗疾病的发生和进展。我们利用环境毒素诱导的果蝇帕金森病(PD)模型作为一种廉价的体内筛选平台,来探索选定膳食类黄酮的神经保护潜力。我们已经确定了一组特定的类黄酮,称为黄酮类化合物,它们对百草枯(PQ)诱导的神经退行性表型具有保护作用,包括生存能力降低、运动缺陷和氧化应激增强。有趣的是,研究的其他类黄酮组,即黄酮类化合物和黄酮醇类化合物,未能提供保护作用,这表明需要特定的结构特征来赋予果蝇对 PQ 介导的神经毒性的保护作用。根据我们的筛选结果,具有神经保护作用的黄酮类化合物在 C3 位没有功能基团取代,并且含有α,β-不饱和羰基。此外,黄酮类化合物介导的神经保护作用不仅依赖于核因子红细胞 2 相关因子 2(Nrf2)的抗氧化特性,还需要调节免疫缺陷(IMD)途径,涉及 NFκB 和敲入(Pirk)后负调节不良的 IMD 反应。我们的数据确定了特定的类黄酮结构特征,这些特征为环境毒素诱导的 PD 发病机制提供了神经保护作用,可以探索新的治疗干预措施。