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家蚕茧丝叶黄素提取物对β-淀粉样肽诱导的 PC12 细胞凋亡的保护作用。

Protective effects of silk lutein extract from Bombyx mori cocoons on β-Amyloid peptide-induced apoptosis in PC12 cells.

机构信息

Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.

Department of Anatomy, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand; Center for Research and Development of Natural Products for Health, Chiang Mai University.

出版信息

Biomed Pharmacother. 2018 Jul;103:582-587. doi: 10.1016/j.biopha.2018.04.045. Epub 2018 Apr 24.

DOI:10.1016/j.biopha.2018.04.045
PMID:29677545
Abstract

Beta-amyloid (Aβ) peptide, the hallmark of Alzheimer's disease (AD), invokes a cascade of oxidative damage to neurons and eventually leads to neuronal death. This study evaluated the protective effects of lutein extract from yellow cocoons of Bombyx mori, and its underlying mechanisms against was investigated to assess its protective effects and the underlying mechanisms against Aβ-induced neuronal cell death in cultured rat pheochromocytoma (PC12) cells. Aβ-induced neuronal toxicity is characterized by decrease in cell viability, increase in intracellular reactive oxygen species (ROS) production, activation of mitochondrial death pathway, and activation the phospholyration of mitogen-activated protein kinase (MAPKs) pathway. Pretreatment with silk lutein extract significantly attenuated Aβ-induced loss of cell viability, apoptosis, MAPKs pathway activation and ROS production. Taken together, our present study suggests that silk lutein extract protects PC12 cells from Aβ-induced neurotoxicity via the reduction of the ROS production, and subsequent attenuation of the mitochondrial death pathway and reduces the activation of the MAPK kinase pathways. This compound might beneficial as potential therapeutic agent to prevent or retard the development and progression of AD.

摘要

β-淀粉样肽(Aβ)是阿尔茨海默病(AD)的标志性物质,它引发了一连串的神经元氧化损伤,最终导致神经元死亡。本研究评估了黄色蚕茧中提取的叶黄素对神经元的保护作用,并研究了其潜在机制,以评估其对 Aβ诱导的培养大鼠嗜铬细胞瘤(PC12)细胞死亡的保护作用和潜在机制。Aβ诱导的神经元毒性表现为细胞活力下降、细胞内活性氧(ROS)生成增加、线粒体死亡途径激活以及丝裂原激活蛋白激酶(MAPKs)途径磷酸化激活。用丝肽叶黄素提取物预处理可显著减轻 Aβ诱导的细胞活力丧失、细胞凋亡、MAPKs 途径激活和 ROS 生成。综上所述,我们的研究表明,丝肽叶黄素提取物通过减少 ROS 生成,减轻线粒体死亡途径和减少 MAPK 激酶途径的激活,从而保护 PC12 细胞免受 Aβ诱导的神经毒性。这种化合物可能作为预防或延缓 AD 发展和进展的潜在治疗剂有益。

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