Kongsui Ratchaniporn, Promsrisuk Tichanon, Klimaschewski Lars, Sriraksa Napatr, Jittiwat Jinatta, Thongrong Sitthisak
Division of Physiology, School of Medical Sciences, University of Phayao, Mueang Phayao District, Phayao, 56000, Thailand.
Division of Neuroanatomy, Department of Anatomy Histology and Embryology, Innsbruck Medical University, Innsbruck, 6020, Austria.
F1000Res. 2023 Oct 27;12:846. doi: 10.12688/f1000research.134891.2. eCollection 2023.
: One of the most common neurodegenerative diseases is Parkinson's disease (PD); PD is characterized by a reduction of neurons containing dopamine in the substantia nigra (SN), which leads to a lack of dopamine (DA) in nigrostriatal pathways, resulting in motor function disorders. Oxidative stress is considered as one of the etiologies involved in dopaminergic neuronal loss. Thus, we aimed to investigate the neuroprotective effects of pinostrobin (PB), a bioflavonoid extracted from with antioxidative activity in PD. : Rats were treated with 40 mg/kg of PB for seven consecutive days before and after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD. After completing the experiment, the brains including SN and striatum were used for histological studies and biochemical assays. : PB treatment demonstrated a reduction of free radicals in the SN as indicated by significantly decreased MDA levels, whereas the antioxidative enzymes (SOD and GSH) were significantly increased. Furthermore, PB treatment significantly increased glial cell line-derived neurotrophic factor (GDNF) immunolabelling which has neurotrophic and neuroprotective effects on the survival of dopaminergic neurons. Furthermore, PB treatment was shown to protect CA1 and CA3 neurons in the hippocampus and dopaminergic neurons in the SN. DA levels in the SN were increased after PB treatment, leading to the improvement of motor function of PD rats. : These results imply that PB prevents MPTP-induced neurotoxicity via its antioxidant activities and increases GDNF levels, which may contribute to the therapeutic strategy for PD.
最常见的神经退行性疾病之一是帕金森病（PD）；PD的特征是黑质（SN）中含多巴胺的神经元减少，这导致黑质纹状体通路中多巴胺（DA）缺乏，从而导致运动功能障碍。氧化应激被认为是多巴胺能神经元丢失的病因之一。因此，我们旨在研究白杨素（PB）的神经保护作用，PB是一种从具有抗氧化活性的物质中提取的生物黄酮，用于治疗PD。：在1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的PD前后，大鼠连续7天接受40mg/kg的PB治疗。实验完成后，将包括SN和纹状体的大脑用于组织学研究和生化分析。：PB治疗显示SN中的自由基减少，MDA水平显著降低，而抗氧化酶（SOD和GSH）显著增加。此外，PB治疗显著增加了胶质细胞源性神经营养因子（GDNF）的免疫标记，GDNF对多巴胺能神经元的存活具有神经营养和神经保护作用。此外，PB治疗显示可保护海马中的CA1和CA3神经元以及SN中的多巴胺能神经元。PB治疗后SN中的DA水平升高，导致PD大鼠运动功能改善。：这些结果表明，PB通过其抗氧化活性预防MPTP诱导的神经毒性并增加GDNF水平，这可能有助于PD的治疗策略。
