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  1. NTU Theses and Dissertations Repository
  2. 醫學院
  3. 毒理學研究所
請用此 Handle URI 來引用此文件: http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/41475
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dc.contributor.advisor劉興華(Shing-Hwa Liu)
dc.contributor.authorTung-Ying Luen
dc.contributor.author呂東穎zh_TW
dc.date.accessioned2021-06-15T00:20:15Z-
dc.date.available2011-02-17
dc.date.copyright2009-02-17
dc.date.issued2009
dc.date.submitted2009-02-10
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dc.identifier.urihttp://tdr.lib.ntu.edu.tw/jspui/handle/123456789/41475-
dc.description.abstract骨質疏鬆症一般被認為是細胞的骨生成作用與破骨細胞的骨吸收作用失去平衡,然而近年來的研究指出骨頭內的間質幹細胞分化成造骨細胞的能力減弱或是間質幹細胞分化成脂肪細胞的能力增強,這樣的結果往往會導致骨質疏鬆症,如糖尿病狀態。 砷為環境中普遍存在的毒性危害物質,我們的水源、空氣包括生物體內都有存在砷,因此人們很容易暴露到砷,砷主要經呼吸、皮膚及消化道吸收,進而 分佈於我們的組織和器官而造成傷害,如皮膚和骨頭,但過去的研究鮮少去探討砷會於骨生成的影響。 因此,本篇主是探討砷化物中的三氧化二砷對於間質幹細胞分化成造骨細胞和脂肪細胞的影響。首先我們選定了不造成細胞死亡的劑量:0.5 μM和1 μM,在此劑量下我們發現三氧化二砷會透過抑制AMPK、eNOS、BMP-2、ALP和OCN的表現來達到抑制骨生成,三氧化二砷對於脂肪細胞分化方面,0.5 μM及1 μM三氧化二砷有促進脂肪細胞分化的現象,而我們也發現在此劑量下三氧化二砷會透過ERK的磷酸化促進脂肪細胞的分化和抑制骨礦物化。在動物實驗上,我們將1 μM三氧化二砷在大鼠脛骨作局部注射和以0.5 ppm和5 ppm三氧化二砷水溶液對鼷鼠連續餵食六週,發現經三氧化二砷處理後,經細胞分化測試、骨密度測定和骨組織切片看到實驗動物的骨生成受到抑制。
綜合以上實驗結果,我們認為三氧化二砷0.5及1 μM劑量下有助於MSCs趨向分化成脂肪細胞同時也抑制了骨生成。
zh_TW
dc.description.abstractIn general, osteoporosis is a disease of bone which is caused by an imbalance between osteoblastic bone formation and osteoclastic bone resorption. However, the recent research showed that the ability of bone marrow mesenchymal stem cells differentiates into adipocytes is greater than osteoblasts and it was thought to cause into osteoporosis, such as diabetes. Arsenic is a common environmental toxicant including in water and air, and we expose to arsenic easily. Arsenic is mainly absorbed via breathing, skin and digestive tract, and then it distributes into our tissues and organs, such as skin and bone. However, few studies show the effects of arsenic to bone. Here we used arsenic trioxide to understand how it affects osteogenesis and adipogenesis of bone marrow mesenchymal stem cells. At first, we selected the arsenic trioxide dose(0.5 μM and 1 μM) that do not cause MSCs death. After 0.5 μM and 1 μM arsenic trioxide treatment, we found that arsenic trioxide inhibited bone formation via decreasing the expressions of AMPK、eNOS、BMP-2、ALP and OCN. Moreover, we also found that 0.5 μM and 1 μM arsenic trioxide can increase adipocyte differentiation and depressed bone formation via the phosphorylation of ERK. In animal test, we injected 1 μM arsenic trioxide into the tibia of rats and fed 0.5 and 5 ppm arsenic trioxide to mice for 6 weeks. The data of BMD, cell differentiation, and slices show the ability of bone formation in animal was inhibited. In Conclusion, we thought that 0.5 μM and 1 μM arsenic trioxide help MSCs favor adipogenesis and it also inhibited osteogenesis.en
dc.description.provenanceMade available in DSpace on 2021-06-15T00:20:15Z (GMT). No. of bitstreams: 1
ntu-98-R95447005-1.pdf: 1495786 bytes, checksum: 0a67da4757afd46b120de9bc2894d99f (MD5)
Previous issue date: 2009
en
dc.description.tableofcontents目錄....................................3
中文摘要............................4
英文摘要............................6
縮寫表.................................8
第一章 緒論.....................10
第二章 材料與方法.........20
第三章 結果......................30
第四章 討論.......................36
附圖.......................................42
參考文獻...............................64
dc.language.isozh-TW
dc.subject骨質酥鬆症zh_TW
dc.subject造骨細胞分化zh_TW
dc.subject間質幹細胞zh_TW
dc.subject脂肪細胞分化zh_TW
dc.subject三氧化二砷zh_TW
dc.subjectosteogenesisen
dc.subjectmesenchymal stem cellsen
dc.subjectadipogenesisen
dc.subjectosteoporosis and arsenic trioxideen
dc.title三氧化二砷對於骨髓間質幹細胞分化成造骨
細胞和脂肪細胞的影響
zh_TW
dc.titleEffects of Arsenic Trioxide on Osteogenesis and Adipogenesis from Bone Marrow Mesenchymal Stem Cellsen
dc.typeThesis
dc.date.schoolyear97-1
dc.description.degree碩士
dc.contributor.oralexamcommittee楊榮森(Rong-Sen Yang),蕭水銀(Shoei-Yn Lin-Shiau)
dc.subject.keyword間質幹細胞,造骨細胞分化,脂肪細胞分化,骨質酥鬆症,三氧化二砷,zh_TW
dc.subject.keywordmesenchymal stem cells,adipogenesis,osteogenesis,osteoporosis and arsenic trioxide,en
dc.relation.page70
dc.rights.note有償授權
dc.date.accepted2009-02-10
dc.contributor.author-college醫學院zh_TW
dc.contributor.author-dept毒理學研究所zh_TW
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