Angelopoulou Efthalia, Nath Paudel Yam, Piperi Christina, Mishra Awanish
Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
Neuropharmacology Research Strength, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Subang Jaya, Malaysia.
J Biochem Mol Toxicol. 2021 Feb 15:e22711. doi: 10.1002/jbt.22711.
Parkinson's disease (PD) is the most common neurodegenerative movement disorder with obscure etiology and no disease-modifying therapy to date. Hence, novel, safe, and low cost-effective approaches employing medicinal plants are currently receiving increased attention. A growing body of evidence has revealed that cinnamon, being widely used as a spice of unique flavor and aroma, may exert neuroprotective effects in several neurodegenerative diseases, including PD. In vitro evidence has indicated that the essential oils of Cinnamomum species, mainly cinnamaldehyde and sodium benzoate, may protect against oxidative stress-induced cell death, reactive oxygen species generation, and autophagy dysregulation, thus acting in a potentially neuroprotective manner. In vivo evidence has demonstrated that oral administration of cinnamon powder and sodium benzoate may protect against dopaminergic cell death, striatal neurotransmitter dysregulation, and motor deficits in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse models of PD. The underlying mechanisms of its action include autophagy regulation, antioxidant effects, upregulation of Parkin, DJ-1, glial cell line-derived neurotrophic factor, as well as modulation of the Toll-like receptors/nuclear factor-κB pathway and inhibition of the excessive proinflammatory responses. In addition, in vitro and in vivo studies have shown that cinnamon extracts may affect the oligomerization process and aggregation of α-synuclein. Herein, we discuss recent evidence on the novel therapeutic opportunities of this phytochemical against PD, indicating additional mechanistic aspects that should be explored and potential obstacles/limitations that need to be overcome for its inclusion in experimental PD therapeutics.
帕金森病（PD）是最常见的神经退行性运动障碍，病因不明，迄今为止尚无改变疾病进程的治疗方法。因此，采用药用植物的新颖、安全且低成本高效益的方法目前正受到越来越多的关注。越来越多的证据表明，肉桂作为一种具有独特风味和香气的香料被广泛使用，可能对包括PD在内的几种神经退行性疾病发挥神经保护作用。体外证据表明，樟属植物的精油，主要是肉桂醛和苯甲酸钠，可能预防氧化应激诱导的细胞死亡、活性氧生成和自噬失调，从而以潜在的神经保护方式发挥作用。体内证据表明，口服肉桂粉和苯甲酸钠可能预防1-甲基-4-苯基-1,2,3,6-四氢吡啶PD小鼠模型中的多巴胺能细胞死亡、纹状体神经递质失调和运动功能障碍。其作用的潜在机制包括自噬调节、抗氧化作用、帕金蛋白、DJ-1、胶质细胞源性神经营养因子的上调，以及Toll样受体/核因子-κB途径的调节和过度促炎反应的抑制。此外，体外和体内研究表明，肉桂提取物可能影响α-突触核蛋白的寡聚化过程和聚集。在此，我们讨论了这种植物化学物质针对PD的新治疗机会的最新证据，指出了应探索的其他机制方面以及将其纳入实验性PD治疗中需要克服的潜在障碍/限制。
