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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
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dc.contributor.advisor | 潘敏雄(Min-Hsiung Pan) | |
dc.contributor.author | Tzu-Li Huang | en |
dc.contributor.author | 黃孜立 | zh_TW |
dc.date.accessioned | 2021-05-19T17:56:28Z | - |
dc.date.available | 2021-09-08 | |
dc.date.available | 2021-05-19T17:56:28Z | - |
dc.date.copyright | 2016-09-08 | |
dc.date.issued | 2016 | |
dc.date.submitted | 2016-08-17 | |
dc.identifier.citation | 張如華, 近十年全球茶葉產銷概況. 茶業專訊. 2012, 30, 29-34.
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dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/7864 | - |
dc.description.abstract | 甲基乙二醛 (methylglyoxal, MG) 為一種高反應活性的雙羰基醛類化合物,已有許多研究證實MG造成神經損傷進一步導致神經退化性疾病的發生。茶葉是一種傳統的飲品,流行病學研究指出,長期飲茶能有效降低罹患神經退化性疾病的風險。文獻提出綠茶中的主要活性物質:表沒食子兒茶素沒食子酸酯「(-)-epigallocatechin-3-gallate, EGCG」以及烏龍茶經發酵後產生的EGCG二聚物: 聚酯型兒茶素A (theasinensin A, TSA) 具有抗氧化等功效,然而其在神經保護之功效與分子機制仍不清楚。因此,本篇研究擬以人類神經瘤細胞SH-SY5Y探討茶多酚EGCG以及TSA對於MG誘導的神經毒性之保護作用及其分子機轉。本研究顯示,EGCG與TSA對於MG誘導的神經毒性具有相當的保護效果。EGCG與TSA皆可透過阻斷MG誘導之活性氧物質 (reactive oxygen species, ROS) 產生以及維持胞內GSH含量,藉此減少MG誘導的氧化壓力。透過caspase 3活化及其基質PARP降解可知EGCG能抑制MG誘導之細胞凋亡現象,然而TSA抑制MG誘導細胞凋亡現象並不顯著。透過acridine orange (AO) 染色於共軛焦顯微鏡下觀察、AO染色後透過流式細胞儀測量螢光強度以及LC3蛋白質的表現判斷MG在TSA存在下會促使細胞走向自噬作用進而保護神經細胞。在MG誘導神經毒性之情形下,EGCG抑制p53、MAPK訊息傳遞路徑進而抑制細胞凋亡,另一方面TSA透過抑制Akt訊息傳遞路徑達到促進細胞自噬作用之功效。綜合上述發現在MG誘導之神經細胞死亡中 EGCG和TSA扮演不同角色與功能,EGCG透過抑制MG誘導的細胞凋亡而TSA則是透過誘發細胞自噬進而保護細胞免於MG誘導的細胞毒性。我們期望此研究成果未來能提供茶多酚開發為預防MG誘導神經相關疾病發展之重要依據。 | zh_TW |
dc.description.abstract | Methylglyoxal (MG) is a highly reactive dicarbonyl aldehyde. MG has been proved to be toxic to neuron and may be the reason of many neurodegenerative diseases. Tea is a traditional drinking and previous studies have observed that chronic tea consumption may reduce the risk of neurodegeneration. One of the most well-known tea catechin, (-)-epigallocatechin-3-gallate (EGCG), and theasinensin A (TSA), the dimer of EGCG had been found to have many bioactivities, such as anti-oxidation. However, the effect of the neuroprotective effect of tea polyphenol remains unclear. The aim of this study is to investigate the neuroprotective effects and the molecular mechanism of tea polyphenol against MG-induced toxicity in SH-SY5Y cell model. The cell viability assay demonstrated that EGCG and TSA treatment protected cells from MG-induced neurotoxicity. Besides, evidences from flow cytometry showed that EGCG and TSA inhibited MG-induced oxidative stress via reducing MG-induced reactive oxygen species (ROS) generation and induce intracellular GSH level. Through activation of caspase 3 and cleavage-PARP, EGCG would inhibit MG-induced apoptosis but TSA did not inhibit MG-induced apoptosis. The result of acridine orange (AO) stain, detecting AO fluoresce intensity and the level of LC3, showed that TSA would induce autophagy in MG-treated neuron cell. EGCG inhibited p53 and MAPK pathway to increase cell viability via western blotting analysis; on the other hand, TSA inhibited Akt pathway to induce autophagy. In conclusion, both EGCG and TSA has the ability to protect cell from MG-induced cytotoxicity via different mechanisms. We expect that EGCG and TSA could be reagents to protect neurodegenerative diseases. | en |
dc.description.provenance | Made available in DSpace on 2021-05-19T17:56:28Z (GMT). No. of bitstreams: 1 ntu-105-R03641036-1.pdf: 5691616 bytes, checksum: 880a82a9195254e5e174887cf7fd3680 (MD5) Previous issue date: 2016 | en |
dc.description.tableofcontents | 謝誌 i
中文摘要 iii Abstract iv 目錄 v 附圖目錄 viii 圖目錄 x 縮寫表 xi 第一章 前言 1 第二章 文獻回顧 3 第一節 甲基乙二醛 (methylglyoxal, MG) 3 (一) 結構 3 (二) 內生性與外生性來源 3 (三) 蛋白質修飾作用與糖化終產物之形成 5 (四) MG所造成的細胞損傷 6 (五) 對生物體的傷害 7 第二節 活性氧分子 (reactive oxygen species, ROS) 10 (一) 活性氧分子與氧化壓力 (oxidative stress) 10 (二) 抗氧化防禦系統 11 第三節 細胞死亡的途徑及保護機制 13 (一) 細胞凋亡 (apoptosis) 14 (二) 細胞自噬 (autophagy) 16 (三) 細胞凋亡與細胞自噬之間的交互作用 19 第四節 茶葉及其發酵產物介紹 23 (一) 茶葉 23 (二) 表沒食子兒茶素沒食子酸酯 ( (-) – Epigallocatechin – 3 - gallate, EGCG) 24 (三) 聚酯型兒茶素A (Theasinensin A, TSA) 25 第三章 實驗目的及架構 28 第一節 實驗目的 28 第二節 實驗架構 29 第四章 實驗材料及方法 30 第一節 實驗材料 30 (一) 樣品試劑 30 (二) 儀器設備 33 第二節 樣品製備 35 (一) 樣品來源 35 (二) 合成原理 35 (三) 實驗步驟 35 (四) 製備 38 第三節 細胞培養 39 (一) 細胞株 39 (二) 試劑配置 39 (三) 解凍 39 (四) 繼代 40 (五) 凍管 40 第四節 細胞存活率分析 (MTT assay) 41 第五節 胞內ROS產生量分析 43 第六節 GSH含量測定分析 45 第七節 AO染色分析 46 第八節 細胞自噬分析 48 第九節 蛋白質電泳 (SDS-PAGE) 與西方墨點法 (Western blotting) 49 第十節 粒線體膜電位分析 54 第十一節 統計分析 55 第五章 實驗結果 56 第一節 茶多酚對於MG誘導神經細胞株毒性之保護效果 56 第二節 茶多酚抑制MG誘導之胞內ROS含量 57 第三節 EGCG抑制MG所誘導之細胞凋亡 57 第四節 TSA誘發細胞自噬保護MG所誘導之神經毒性 57 第五節 茶多酚抑制MG誘導神經毒性之分子機轉 58 第六章 討論 60 第七章 結論 64 第八章 圖表 65 參考文獻 82 | |
dc.language.iso | zh-TW | |
dc.title | 茶多酚對甲基乙二醛誘導人類神經細胞毒性之保護功效 | zh_TW |
dc.title | The Protective Effect of Tea Polyphenol against Methylglyoxal-induced Neurotoxicity | en |
dc.type | Thesis | |
dc.date.schoolyear | 104-2 | |
dc.description.degree | 碩士 | |
dc.contributor.coadvisor | 李銘仁(Ming-Jen Lee) | |
dc.contributor.oralexamcommittee | 何其儻(Chi-Tang Ho),陳宏彰,何元順 | |
dc.subject.keyword | 甲基乙二醛,表沒食子兒茶素沒食子酸酯,聚酯型兒茶素A,細胞凋亡,細胞自噬,氧化壓力, | zh_TW |
dc.subject.keyword | Methylglyoxal (MG),(-)-Epigallocatechin-3-gallate (EGCG),Theasinensin A (TSA),Apoptosis,Autophagy,Oxidative stress, | en |
dc.relation.page | 136 | |
dc.identifier.doi | 10.6342/NTU201603033 | |
dc.rights.note | 同意授權(全球公開) | |
dc.date.accepted | 2016-08-19 | |
dc.contributor.author-college | 生物資源暨農學院 | zh_TW |
dc.contributor.author-dept | 食品科技研究所 | zh_TW |
顯示於系所單位: | 食品科技研究所 |
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ntu-105-1.pdf | 5.56 MB | Adobe PDF | 檢視/開啟 |
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