Neuroprotective effect of green tea extract (-)-epigallocatechin-3-gallate in a preformed fibril-induced mouse model of Parkinson's disease.

IF 1.6 4区 医学 Q4 NEUROSCIENCES Neuroreport Pub Date : 2024-04-03 Epub Date: 2024-03-07 DOI:10.1097/WNR.0000000000002027
Jianing Shen, Junhua Xie, Liyuan Ye, Jian Mao, Shihao Sun, Weiwei Chen, Sijia Wei, Sisi Ruan, Linhai Wang, Hangcui Hu, Jingjing Wei, Yao Zheng, Zhouyan Xi, Ke Wang, Yan Xu
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Abstract

Parkinson's disease (PD) is the second most common neurodegenerative disease characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra (SN). The main bioactive component of green tea polyphenols (-)-epigallocatechin-3-gallate (EGCG) exerts protective effects against diseases such as neurodegenerative diseases and cancer. Therefore, this study investigated the effect of EGCG on the amelioration of neural damage in a chronic PD mouse model induced by α-synuclein preformed fibrils (α-syn-PFFs). A total of 20 C57BL/6J female mice were randomly divided into 3 groups: control group (saline, n = 6), model group (PFFs, n = 7), and prevention group (EGCG+PFFs, n = 7). A chronic PD mouse model was obtained by the administration of α-syn-PFFs by stereotaxic localization in the striatum. Behavioral tests were performed to evaluate PD-related anxiety-like behavior and motor impairments in the long-term PD progression. Tyrosine hydroxylase (TH) immuno-positive neurons and Ser129-phosphorylated α-syn (p-α-syn) were identified by immunohistochemistry. Pro-inflammatory and anti-inflammatory cytokines were measured by real-time quantitative PCR. EGCG pretreatment reduced anxiety-like behavior and motor impairments as revealed by the long-term behavioral test (2 weeks, 1 month, 3 months, and 6 months) on PD mice. EGCG also ameliorated PFF-induced degeneration of TH immuno-positive neurons and accumulation of p-α-syn in the SN and striatum at 6 months. Additionally, EGCG reduced the expression of pro-inflammatory cytokines while promoting the release of anti-inflammatory cytokines. EGCG exerts a neuroprotective effect on long-term progression of the PD model.

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绿茶提取物(-)-表没食子儿茶素-3-棓酸盐对预成纤维诱导的帕金森病小鼠模型的神经保护作用。
帕金森病(PD)是第二大常见的神经退行性疾病,其特征是黑质(SN)中的多巴胺能神经元逐渐退化。绿茶多酚的主要生物活性成分(-)-表没食子儿茶素-3-棓酸盐(EGCG)对神经退行性疾病和癌症等疾病具有保护作用。因此,本研究探讨了 EGCG 对α-突触核蛋白预成纤维(α-syn-PFFs)诱导的慢性帕金森病小鼠模型神经损伤的改善作用。将20只C57BL/6J雌性小鼠随机分为3组:对照组(生理盐水,n = 6)、模型组(PFFs,n = 7)和预防组(EGCG+PFFs,n = 7)。慢性帕金森氏症小鼠模型是通过在纹状体中进行立体定位给药α-syn-PFFs而获得的。行为测试用于评估与帕金森病相关的焦虑样行为和帕金森病长期进展过程中的运动障碍。通过免疫组化鉴定了酪氨酸羟化酶(TH)免疫阳性神经元和Ser129磷酸化的α-syn(p-α-syn)。通过实时定量 PCR 检测促炎和抗炎细胞因子。对帕金森病小鼠进行的长期行为测试(2周、1个月、3个月和6个月)显示,EGCG预处理可减少焦虑样行为和运动障碍。6个月时,EGCG还能改善PFF诱导的TH免疫阳性神经元变性以及p-α-syn在SN和纹状体中的积累。此外,EGCG 还能减少促炎细胞因子的表达,同时促进抗炎细胞因子的释放。EGCG对帕金森病模型的长期进展具有神经保护作用。
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来源期刊
Neuroreport
Neuroreport 医学-神经科学
CiteScore
3.20
自引率
0.00%
发文量
150
审稿时长
1 months
期刊介绍: NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool. The core interest of the Journal is on studies that cast light on how the brain (and the whole of the nervous system) works. We aim to give authors a decision on their submission within 2-5 weeks, and all accepted articles appear in the next issue to press.
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