BioISI─Biosystems and Integrative Sciences Institute, Faculty of Sciences of the University of Lisbon, C8, Campo Grande, Lisbon 1749-016, Portugal.
ACS Chem Neurosci. 2023 May 17;14(10):1905-1920. doi: 10.1021/acschemneuro.3c00162. Epub 2023 Apr 26.
While several polyphenols were found to either inhibit or modulate the aggregation of proteins implicated in neurodegenerative diseases, such as Parkinson's disease (PD), discrepant action mechanisms have been reported. This, in addition to some polyphenols' pan-assay interference compounds' reputation, casts some doubts concerning their therapeutic relevance. Here, we studied, through molecular dynamics and enhanced sampling methods, the aggregation of 11-mer peptides from the non-amyloid-β component, an aggregation-prone domain of α-synuclein (α-syn) implicated in PD and other synucleinopathies, in neat water and aqueous solutions of resveratrol (RSV) and gallic acid (GA). Further, simulations of the complete protein were carried out in aqueous urea, RSV, and GA solutions. Our results show that peptide aggregation is not disrupted by either phenolic compound. Thus, instead, intrusion of RSV and GA in the inter-peptide region induces a peptide-peptide re-orientation, favoring terminal interactions that manifest in the formation of barrierless solvent-separated configurations. Moreover, although the (poly)phenols induce a pronounced peptide dewetting at high concentrations, β-sheet-rich regions, a hallmark of α-syn aggregation, are not disrupted. Thus, our results indicate that, if anything, RSV and GA delay or modulate peptide aggregation at high concentrations via the stabilization of solvent-separated conformations as opposed to aggregation inhibition. Structural analysis of the full protein, however, shows that the (poly)phenols induce more extended conformations of α-syn, similar to urea, possibly also influencing its aggregation propensity. However, opposite to urea, the (poly)phenols reduce α-syn's conformational space, likely due to steric effects and a slowdown of the solvent dynamics. These effects are concentration-dependent and possibly unattainable at therapeutic-relevant concentrations. These results suggest that the aggregation inhibition activity of RSV and GA in vitro should involve, instead, either the non-covalent binding to oligomeric intermediates or the stabilization of the monomer and/or oligomers through the formation of covalent bonds of the respective quinones with α-syn. In addition, the enhanced aggregation tendency of the peptides observed here could be associated with the formation of non-toxic oligomers, reported for some polyphenols.
虽然已经发现几种多酚可以抑制或调节与神经退行性疾病(如帕金森病)相关的蛋白质聚集,如帕金森病(PD),但已经报道了不同的作用机制。此外,一些多酚被认为是 pan-assay interference compounds,这使得人们对它们的治疗相关性产生了一些怀疑。在这里,我们通过分子动力学和增强采样方法研究了 11 肽从非淀粉样β成分的聚集,非淀粉样β成分是 α-突触核蛋白(α-syn)的一个易于聚集的结构域,与 PD 和其他突触核蛋白病有关,在纯净水中和白藜芦醇(RSV)和没食子酸(GA)的水溶液中。此外,还在水合脲、RSV 和 GA 溶液中进行了完整蛋白质的模拟。我们的结果表明,多酚化合物不会破坏肽的聚集。因此,相反,RSV 和 GA 侵入肽间区域会引起肽-肽重新取向,有利于末端相互作用,从而形成无阻碍的溶剂分离构型。此外,尽管(多)酚在高浓度下会显著使肽去润湿,但不会破坏富含β-折叠的区域,这是 α-syn 聚集的一个标志。因此,我们的结果表明,如果有的话,RSV 和 GA 会通过稳定溶剂分离的构象来延迟或调节高浓度下的肽聚集,而不是抑制聚集。然而,与尿素相反,(多)酚会使 α-syn 呈现出更伸展的构象,类似于尿素,这可能也会影响其聚集倾向。然而,与尿素相反,(多)酚会降低 α-syn 的构象空间,可能是由于空间位阻效应和溶剂动力学的减慢。这些影响与浓度有关,在治疗相关浓度下可能无法实现。这些结果表明,RSV 和 GA 在体外抑制聚集的活性可能涉及与寡聚中间体的非共价结合,或者通过形成相应的醌与 α-syn 的共价键来稳定单体和/或寡聚物。此外,这里观察到的肽的增强聚集趋势可能与一些多酚形成非毒性寡聚物有关。