Ginkgo biloba Extract Improves Dendritic Spine Injury in Cerebellar Purkinje Cells Induced by MPTP in Mice by Regulating the PLK2-SPAR Pathway.

IF 1.6 4区 医学 Q4 NEUROSCIENCES
Synapse Pub Date : 2025-03-01 DOI:10.1002/syn.70013
Yilin Lyu, Yumei Zhang
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引用次数: 0

Abstract

Parkinson's disease (PD) is a common neurodegenerative disease, and, currently, there is no cure for patients with PD. Studies have shown that Ginkgo biloba extract (EGb) has good neuroprotective effects against PD. The cerebellum is widely involved in cognitive function and may be related to the regulation of static tremors in PD. However, research on the corresponding microstructures is limited. Purkinje cells (PCs) are the only efferent neurons present in the cerebellum, and dendritic spines in PCs are considered the key structures for transmitting neuronal excitatory signals. When neurons are activated, polo-like kinase 2 (PLK2) is expressed, leading to the degradation of spine-associated Rap guanosine triphosphatase activating protein (SPAR) and, ultimately, the loss of postsynaptic density protein 95 (PSD-95), causing changes in the morphology or quantity of dendritic spines. This raises the question of whether the neuroprotective effect of EGb involves the PLK2-SPAR pathway. In this study, we used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to establish a mouse model of dopamine neuronal injury. Golgi staining was performed to observe the dendritic spine changes. Immunohistochemistry was used to detect the expression of PLK2, SPAR, and PSD-95. The results showed that EGb improves MPTP-induced behavioral changes, dopamine neuronal injury, and dendritic spine damage in mice. In addition, EGb reversed the changes in PLK2, SPAR, and PSD-95 expressions caused by MPTP, revealing the potential mechanism by which EGb improves the condition of patients with PD.

银杏叶提取物通过调节PLK2-SPAR通路改善MPTP诱导小鼠小脑浦肯野细胞树突状脊柱损伤
帕金森病(PD)是一种常见的神经退行性疾病,目前还没有治愈PD患者的方法。研究表明,银杏叶提取物(EGb)对帕金森病具有良好的神经保护作用。小脑广泛参与认知功能,并可能与PD静态震颤的调节有关。然而,对其微观结构的研究是有限的。浦肯野细胞(Purkinje cells, PCs)是小脑中唯一存在的传出神经元,其树突棘被认为是传递神经元兴奋性信号的关键结构。当神经元被激活时,polo样激酶2 (PLK2)表达,导致脊柱相关Rap鸟苷三磷酸酶激活蛋白(SPAR)的降解,最终导致突触后密度蛋白95 (PSD-95)的丢失,导致树突棘形态或数量的改变。这就提出了EGb的神经保护作用是否涉及PLK2-SPAR通路的问题。本研究采用1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)建立小鼠多巴胺神经元损伤模型。高尔基染色观察树突棘的变化。免疫组化检测PLK2、SPAR、PSD-95的表达。结果表明,EGb可改善mptp诱导的小鼠行为改变、多巴胺神经元损伤和树突状脊柱损伤。此外,EGb逆转了MPTP引起的PLK2、SPAR和PSD-95表达的变化,揭示了EGb改善PD患者病情的潜在机制。
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来源期刊
Synapse
Synapse 医学-神经科学
CiteScore
3.80
自引率
0.00%
发文量
38
审稿时长
4-8 weeks
期刊介绍: SYNAPSE publishes articles concerned with all aspects of synaptic structure and function. This includes neurotransmitters, neuropeptides, neuromodulators, receptors, gap junctions, metabolism, plasticity, circuitry, mathematical modeling, ion channels, patch recording, single unit recording, development, behavior, pathology, toxicology, etc.
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