Jiao Panpan, An Yingfeng, Wu Suhui, Li Hanbing, Li Genlin
School of Medicine, Henan University of Chinese Medicine, Zhengzhou, China.
Parkinsons Dis. 2024 Dec 24;2024:9973140. doi: 10.1155/padi/9973140. eCollection 2024.
Cinnamaldehyde (CA), the primary bioactive compound in cinnamon ( Presl, Lauraceae, ), holds potential therapeutic benefits for Parkinson's disease (PD). To scrutinize the impact and mechanisms of CA on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD, male C57BL/6 mice were randomly allocated to CA (150, 300, and 600 mg/kg), model, Madopar, and control group ( = 12). The Open Field, Pole-jump, and Rotarod experiments assessed exercise capacity and anxiety levels. HPLC evaluated the levels of neurotransmitters. Immunohistochemistry was utilized to detect the expression of TH and GFAP. WB and RT-qPCR determine the expression levels of apoptosis-related genes and proteins in the substantia nigra and striatum. The findings revealed that CA not only enhanced motor abilities and reduced anxiety but also elevated the levels of TH, DOPAC, DA, 5-HIAA, HVA, and 5-HT in the substantia nigra and striatum. Moreover, it protected DA neurons and downregulated the expression of , , and mRNA and proteins, while increasing the expression of mRNA compared to the model group. Furthermore, CA was observed to inhibit glial cell activation, leading to reduced levels of GFAP and IBA1 in the substantia nigra and striatum. This resulted in decreased expression of inflammatory factors such as iNOS and NF-Bp65 proteins in these regions, consequently mitigating neuroinflammation. These results suggest that CA exerts a neuroprotective effect in acute PD model mice by suppressing glial cell activation, modulating the expression of apoptotic genes, and alleviating neuroinflammation and apoptosis induced by MPTP.
肉桂醛（CA）是樟科植物肉桂（Presl）中的主要生物活性化合物，对帕金森病（PD）具有潜在的治疗益处。为了研究CA对1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的帕金森病的影响及其机制，将雄性C57BL/6小鼠随机分为CA（150、300和600mg/kg）组、模型组、美多芭组和对照组（每组n = 12）。通过旷场实验、爬杆实验和转棒实验评估运动能力和焦虑水平。采用高效液相色谱法（HPLC）测定神经递质水平。利用免疫组织化学检测酪氨酸羟化酶（TH）和胶质纤维酸性蛋白（GFAP）的表达。通过蛋白质免疫印迹法（WB）和实时定量聚合酶链反应（RT-qPCR）测定黑质和纹状体中凋亡相关基因和蛋白的表达水平。结果显示，CA不仅增强了运动能力、减轻了焦虑，还提高了黑质和纹状体中TH、3,4-二羟基苯乙酸（DOPAC）、多巴胺（DA）、5-羟吲哚乙酸（5-HIAA）、高香草酸（HVA）和5-羟色胺（5-HT）的水平。此外，与模型组相比，CA保护了多巴胺能神经元，下调了Bax、Bcl-2和Caspase-3 mRNA及蛋白的表达，同时增加了Bcl-2 mRNA的表达。此外，观察到CA抑制了胶质细胞的激活，导致黑质和纹状体中GFAP和离子钙结合衔接分子1（IBA1）水平降低。这导致这些区域中诱导型一氧化氮合酶（iNOS）和核因子κB p65（NF-κBp65）蛋白等炎症因子的表达减少，从而减轻了神经炎症。这些结果表明，CA通过抑制胶质细胞激活、调节凋亡基因表达以及减轻MPTP诱导的神经炎症和凋亡，对急性帕金森病模型小鼠发挥神经保护作用。
