利用秀麗隱桿線蟲模型研究水仙?之抗帕金森氏症的效力

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Title:	利用秀麗隱桿線蟲模型研究水仙?之抗帕金森氏症的效力 A study of the antiparkinsonian effects of narcissoside using the pharmacological and transgenic Caenorhabditis elegans models
Authors:	陳妍涓;Yen-Chuan Chen
Contributors:	免疫學研究所碩士班
Keywords:	秀麗隱桿線蟲;水仙?抗帕金森氏症;antiparkinsonian effects;narcissoside;Caenorhabditis elegans
Date:	2018-07-24
Issue Date:	2018-12-25 09:41:44 (UTC+8)
Publisher:	中國醫藥大學
Abstract:	帕金森氏症（PD）是第二種最常見的神經退行性疾病，與患者腦內黑質細胞中α-突觸核蛋白 (α-synuclein) 的聚集和腦中多巴胺 (DA) 神經元的喪失有關。迄今為止，PD沒有有效的治療方法，而利用植化物治療PD的研究已經廣泛的引起了相關研究學者的興趣。本研究中，我們使用秀麗隱桿線蟲（Caenorhabditis elegans）模型探討了從接骨木花（Sambucus nigra flower）中分離得到的化合物：水仙?（Narcissoside），其抗帕金森病性質及其潛在機制。我們證明水仙?可減少6-OHDA所誘導的DA神經元變性，改善食物敏感性行為，並增加因6-OHDA處理所減少的線蟲壽命。同時，水仙?也可減少轉基因秀麗隱桿線蟲模型中的α-突觸核蛋白積累。此外，我們發現藉由促進lgg-1基因的表達增強自噬作用的活性，降低細胞凋亡途徑基因egl-1的表現，以及增加rpn-11基因的表達強化蛋白?體活性可能是水仙?介導的改善PD病理特徵的分子機制。總之，這些發現支持水仙?作為PD治療的可能的治療應用或補充劑，並鼓勵進一步研究水仙?作為有價值的抗神經變性劑。 Parkinson’s disease (PD) is the second frequent neurodegenerative disease that is associated with intracellular α-synuclein (α-Syn) aggregation and ventral midbrain dopaminergic neuronal death in the Substantia Nigra of patients. Presently, there is no successful therapy for PD. The identification and characterization of phytocompounds to treat or cure PD has attracted the interest of the field community.In this research, we investigated compound, narcissoside;(NCS), which is isolated from Sambucus nigra flower (elderflowers)for is anti-Parkinsonian properties, using Caenorhabditis elegans (C. elegans) models and their underlying mechanisms.We demonstrated that NCS reduced 6-hydroxydopamine-induced dopaminergic neuron degeneration, improved food-sensing behavioral abnormalities, and reversed life-span decreases in a pharmacologicalC. elegans model. NCS also diminished α-Syn accumulation in the transgenic C. elegans model. Moreover, we found that enhancement of autophagy activity by promoting lgg-1 expression, down-regulation of the apoptosis pathway gene, egl-1,and increase of proteasome activity by rising rpn-11 expression, may be the molecular mechanism for NCS-mediated protection against PD pathology. Together, these findings support NCS as a possible therapeutic applications or supplements for PD treatment and encourage further investigations of NCS as a valuable anti-neurodegenerative agent.
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