摘要
背景:阿尔茨海默病(AD)是最常见的与年龄相关的痴呆类型。仍然缺乏有效抗淀粉样蛋白β受体 - 蛋白诱导的认知障碍的抗AD药物。 黄芩素是黄芩的主要成分,并具有神经保护特性。在这项研究中,我们提出了进一步深入了解黄芩素在AD病人上的药物作用机制和潜在的靶点。 目的:调查黄芩素在AD动物模型的治疗效果和作用机制。方法:雄性大鼠侧脑室注射淀粉样蛋白β受体(Aβ )1-40,黄连素口服给药。 用Morris水迷宫试验对治疗效果进行了评价,并使用蛋白质组学方法和免疫印迹对作用机理进行了研究。 结果:黄芩素治疗显著减弱Aβ 1-40引起的的认知功能异常。此外,黄芩素显著影响24个蛋白质在大脑皮质和海马的表达水平,这些蛋白质的大约50%是与能量代谢和神经传递有关,而其他均与抗细胞凋亡、抗氧化、应激反应、蛋白质磷酸化、细胞骨架、磷脂代谢和细胞信号传导有关。除了涉及到细胞骨架蛋白,这些蛋白质的表达都增加了,两个蛋白表达的变化通过免疫印迹证实。 结论:黄芩素可改善大鼠Aβ 1-40诱导的痴呆,可能成为一种新的和有前景的用于AD治疗的药物。其治疗机制可能涉及到多个过程的调控,主要是通过促进能量代谢和神经传递,此外也涉及促进抗凋亡、抗氧化、蛋白磷酸化等。
关键词: 阿尔茨海默病,淀粉样蛋白β受体β1-40,黄连素,能量代谢,神经传递,蛋白质组学,空间学习和记忆
Current Alzheimer Research
Title:Ameliorative Effects of Baicalein on an Amyloid-β Induced Alzheimer's Disease Rat Model: A Proteomics Study
Volume: 11 Issue: 9
Author(s): Dongfeng Wei, Jinfu Tang, Weiguo Bai, Yongyan Wang and Zhanjun Zhang
Affiliation:
关键词: 阿尔茨海默病,淀粉样蛋白β受体β1-40,黄连素,能量代谢,神经传递,蛋白质组学,空间学习和记忆
摘要: Background: Alzheimer's disease (AD) is the most common type of age-related dementia. Effective anti-AD drugs against amyloid-β-protein-induced cognitive impairment are still lacking. Baicalein is the main component of Radix Scutellariae and has neuroprotective properties. In this study, we provide further insights into pharmacotherapy mechanisms and potential targets of baicalein in AD. Objective: To investigate the therapeutic effects and mechanism of action of baicalein in an AD rat model. Methods: Male rats were intracerebroventricularly injected with amyloid-β(Aβ) 1-40, and baicalein was orally administered. The therapeutic effect was evaluated with the Morris water maze test, and the mechanism of action was studied using a proteomics approach and western blotting. Results: Baicalein treatment significantly attenuated Aβ1-40-induced abnormalities in cognitive function. Additionally, the expression levels of 24 proteins in the cerebral cortex and hippocampus were significantly influenced by baicalein; approximately 50% of these proteins are related to energy metabolism and neurotransmission, whereas others are related to anti-apoptosis, anti-oxidation, the stress response, protein phosphorylation, the cytoskeleton, phospholipid metabolism and cell signaling. The expression of these proteins was increased, except for the proteins related to the cytoskeleton. The changes in the expression of 2 proteins were confirmed by western blotting. Conclusions: Baicalein ameliorates the Aβ1-40-induced dementia in rats and may be a novel and promising drug for the treatment of AD. The therapeutic mechanism may be related to modulation of a number of processes, mainly through the promotion of energy metabolism and neurotransmission, with the additional promotion of anti-apoptosis, anti-oxidation, protein phosphorylation, etc.
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Cite this article as:
Wei Dongfeng, Tang Jinfu, Bai Weiguo, Wang Yongyan and Zhang Zhanjun, Ameliorative Effects of Baicalein on an Amyloid-β Induced Alzheimer's Disease Rat Model: A Proteomics Study, Current Alzheimer Research 2014; 11 (9) . https://dx.doi.org/10.2174/1567205011666141001113619
DOI https://dx.doi.org/10.2174/1567205011666141001113619 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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