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研究生:朱芷萱
研究生(外文):Chu, Chih-Hsuan
論文名稱:砷在高葡萄糖環境下對於小鼠血管內皮細胞(SVEC4-10) 中氧化應激反應與訊息傳遞路徑之影響
論文名稱(外文):Effects on Oxidative Adaptive Response and Signal Transduction Pathway in Vascular Endothelial Cell (SVEC4-10) Exposed to Arsenic under High Glucose Condition
指導教授:黃登福黃登福引用關係
指導教授(外文):Hwang, Deng-Fwu
口試委員:鄭森雄周薰修陳泰源黃鈺茹
口試委員(外文):Jeng, Sen-ShyongChou, Shin-ShiouChen, Tai-YuanHuang, Yu-Ru
口試日期:2014-06-05
學位類別:碩士
校院名稱:國立臺灣海洋大學
系所名稱:食品科學系
學門:農業科學學門
學類:食品科學類
論文種類:學術論文
論文出版年:2014
畢業學年度:103
語文別:中文
論文頁數:83
中文關鍵詞:糖尿病烏腳病ROS
外文關鍵詞:Arsenicdiabetesblackfoot diseaseROS
相關次數:
  • 被引用被引用:3
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  • 下載下載:60
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砷廣泛存在於環境中,如水、空氣、塵土與食物等。隨著現代人在生活型態與飲食型態的變遷,糖尿病 (diabetes) 的罹患率已逐年攀升。由流行病學研究結果發現,早期臺灣西南部烏腳病流行區域與孟加拉之居民曾處於高濃度砷暴露之環境,而砷與糖尿病有密切關連,且砷 (arsenic) 暴露量與患病率呈劑量正相關性,烏腳病 (blackfoot disease) 屬於周邊血管疾病。本研究以小鼠淋巴結血管內皮細胞株 (SV40 transformation of lymphatic endothelial cells; SVEC4-10) 作為模擬人類血管之模型,並以高濃度葡萄糖模擬糖尿病之環境,添加砷共處理後,觀察兩者是否具協同作用,加劇細胞受到之傷害。在高濃度葡萄糖共培養環境下, SVEC4-10細胞之死亡對於砷具有劑量依賴性。砷會顯著降低粒線體膜電位之螢光強度,增加細胞內活性氧物種 (reactive oxygen species; ROS) 與胞內氧化指標1,2-thiobarbituric acid reactive substances (TBARS) 之含量,改變超氧化物岐化酶 (superoxide dismutase; SOD) 表現量,並使細胞停留於G2期。以促細胞分裂劑活化性蛋白激酶 (mitogen-activated protein kinase; MAPK) 調控酵素c-Jun N-terminal kinase (JNK) 抑制劑SP600125,與細胞外信號調控激酶 (extracellular signal-regulated kinases; ERK) 抑制劑U-0126預處理後,可顯著降低砷在高濃度葡萄糖共培養環境下對於SVEC4-10細胞所誘導之細胞死亡,並回復砷與高濃度葡萄糖所造成粒線體膜電位下降,與增加細胞內ROS之含量。由西方墨點法分析結果得知,砷在高濃度葡萄糖環境下可顯著誘導葡萄糖調節蛋白78 (glucose-regulated protein78; GRP78) 之表現,其為內質網壓力 (Endoplasmic Reticulum Stress; ER stress) 相關調控蛋白。綜合上述結果可知,砷在高濃度葡萄糖環境下可能經由氧化壓力與內質網壓力對於SVEC4-10細胞誘導其細胞死亡,經由JNK與ERK途徑誘導細胞內氧化壓力增加,並造成粒線體損傷、細胞內氧化壓力指標含量增加與抗氧化酵素表現量降低,砷與高濃度葡萄糖對於造成SVEC4-10細胞之氧化傷害具有協同作用。
Arsenic is a naturally occurring and poisonous metalloid element that exists in environmental sources such as air, water, and soil. Endothelial cell toxicity is known that can directly cause endothelial injury and apoptosis. Blackfoot disease is the peripheral vascular disease. The previous studies have shown that blackfoot disease hyperendemic area resident exposed to high level of arsenic in Taiwan and Bangladesh may relate to the development of diabetes. To clarify the molecular mechanisms through which arsenic causes injuries to blood vessels under high glucose condition, SV40 transformation of lymphatic endothelial cells (SVEC4-10) were used to expose to different concentration of arsenic under high glucose (80 mM) condition, and analyzed the oxidative adaptive response in blood vessels and the signal pathway involved in the SVEC4-10 cells. The cells were incubated with different concentrations of arsenic and high glucose (80 mM) for 24 hr, the percentage of cell death was in dose- and time-dependent. It could decrease the mitochondrial membrane potential, and increased the oxidative marker 2-thiobarbituric acid-reactive substances (TBARS) and reactive oxygen species (ROS) production. Arsenic and high glucose would let the cell cycle arrest in G2 phase and change the expression of antioxidant enzyme superoxide dismutase (SOD). Selective blocking of the mitogen-activated protein kinase (MAPK) pathways with c-Jun N-terminal kinase (JNK) inhibitor SP600125 and extracellular signal-regulated kinase (ERK) inhibitor U0126 could significantly decrease arsenic-induced cell death under the high glucose condition. Treatment with arsenic also triggered the expression of endoplasmic reticulum (ER) stress marker, glucose-regulated protein (GRP78) under high glucose conditions. These results showed that oxidative stress and ER stress may be associated with arsenic-induced cytotoxicity under high glucose condition. The assays indicated that arsenic treatment under high glucose condition induced oxidative stress through JNK/ERK pathway in SVEC4-10 cells. The results suggest that arsenic and high glucose may have synergistic effect.
中文摘要 ................................................................................................................... I
Abstract .................................................................................................................. II
壹、文獻整理 ........................................................................................................... 1
一、糖尿病 ....................................................................................................... 2
二、血管疾病 ................................................................................................... 7
三、砷 ............................................................................................................ 12
四、氧化壓力 ................................................................................................. 15
貳、研究內容 ......................................................................................................... 19
第一章、在高葡萄糖培養基中,砷對於 SVEC4-10 細胞所誘導之氧化傷害
一、前言 ......................................................................................................... 20
二、材料與方法 ............................................................................................. 22
三、結果 ......................................................................................................... 28
四、討論 ......................................................................................................... 30
五、圖表 ......................................................................................................... 34
第二章、在高葡萄糖培養基中,砷對於 SVEC4-10 細胞內 MAPK 途徑與內質網
壓力相關途徑之影響
一、前言 ......................................................................................................... 46
二、材料與方法 ............................................................................................. 47
三、結果 ......................................................................................................... 51
四、討論 ......................................................................................................... 53
五、圖表 ......................................................................................................... 55
結 論 ...................................................................................................................... 63
參考文獻 ................................................................................................................ 64
謝 辭 ...................................................................................................................... 79
附 錄 ...................................................................................................................... 80
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