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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 康照洲(Jaw-Jou Kang) | |
| dc.contributor.author | Chun-Ting Juan | en |
| dc.contributor.author | 阮雋婷 | zh_TW |
| dc.date.accessioned | 2021-06-15T04:16:28Z | - |
| dc.date.available | 2014-01-11 | |
| dc.date.copyright | 2010-01-11 | |
| dc.date.issued | 2009 | |
| dc.date.submitted | 2010-01-01 | |
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M., 2004, Heparin-binding epidermal growth factor cleavage mediates zinc-induced epidermal growth factor receptor phosphorylation. American Journal of Respiratory Cell and Molecular Biology. 30(4):540-7. Yoshii, E., 1997, Cytotoxic effects of acrylates and methacrylates: relationships of monomer structures and cytotoxicity. J Biomed Mater Res. 37(4):517-24. Zapolska-Downar, D., A. Zapolski-Downar, M. Markiewski, A. Ciechanowicz, M. Kaczmarczyk, and M. Naruszewicz, 2001, Selective inhibition by probucol of endothelial cells. Atherosclerosis. 155:123-30. Zhang, J., and Zhang, Q. Y., 2009, Application of PI3K/Akt and COX-2 signal pathway blockage in treatment of gastric carcinoma. WJGNET. 17(6): 584-588 賴弘明（2009）。牙周病篩檢新知系列之一: 社區牙周病治療需求指數之應用與詮釋。臺南：臺灣篩檢學會。 葉宏偉（2008）。比較五種傳統與奈米級牙本質黏著劑毒性機轉之探討。國立台灣大學臨床牙醫學研究所碩士論文，未出版。 | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/45368 | - |
| dc.description.abstract | 牙本質黏著劑被廣泛應用在牙科治療上。蛀牙是常見的牙科疾病，主要是由牙菌斑所引起的，牙菌斑會造成牙齦發炎。在過去的研究指出，牙菌斑會誘導前發炎調節蛋白，如腫瘤壞死因子-α(TNF-α)，TNF-α能誘導內皮細胞的發炎相關蛋白ICAM-1 (Intracellular Cell Adhesion Molecule-1) 、 VCAM-1 (Vascular Cell Adhesion Molecule-1) 和環氧化酶-2 (COX-2) ， 因此蛀牙狀態下的牙周組織通常可能發炎 。 牙本質黏著劑在口腔環境中應要保持穩定 ， 但是在聚合作用之後 ， 一些來自黏著材複合樹脂的成分依然會被釋放出來 。 此外並有研究指出 ， 一些合成的牙本質黏著劑會對牙髓造成急性的血管擴張作用 。 由牙本質黏著劑所滲露出的主要成分為單體 ， 像是 BisGMA (bisphenol-glycidyl methacrylate ) 和 HEMA (2-hydroxyethyl methacrylate) 。 關於單體毒性的研究很多 ， 但對於循環系統的作用卻仍不清楚 。 故本研究想了解單體成分對靜脈內皮細胞的發炎作用之影響和可能機制 。 在此研究中 ， 選擇 ICAM-1 、VCAM-1 和 COX-2 這些發炎相關蛋白作研究 ， 並且以初代培養的 HUVECs (Human Umbilical Vein Endothelial Cells ) 作為研究細胞 ， 使用 RT-PCR ( reverse transcriptase PCR ) 和西方墨點分析法觀察 mRNA 和 蛋白質的變化 ， 進一步研究 BisGMA 對 ICAM-1、VCAM-1 和 COX-2 的作用機制。
首先 ， 本研究發現 30μM BisGMA 能誘導 COX-2 蛋白以及 mRNA表現 ， 但是對 ICAM-1 和 VCAM-1 則不具影響 。 此外我們首次發現 BisGMA 誘導 HUVECs 的 COX-2 蛋白表現的途徑 ， 可能分別是透過 EGFR (epidermal growth factor receptor) 到 Akt 之訊息傳遞 ， 以及另一透過 p38 誘導 COX-2 蛋白表現之路徑 。 在第二部分的研究中 ， 我們探討了 HEMA 對發炎相關蛋白的影響 ， 發現 HEMA 對 HUVECs 的 ICAM-1、VCAM-1 和 COX-2 蛋白表現皆沒有影響 ， 然而當以 TNF-α誘導發炎之狀況下 ， 首次發現 0.99 mM 的 HEMA 能抑制 TNF-α所誘導的 ICAM-1、 VCAM-1 和 COX-2 蛋白表現 。 接著為了比較單體和混合物牙本質黏著劑對發炎蛋白的作用是否有正向關聯 ， 我們進一步研究 Voco Solobond M (5th) 與 Voco Futurabond NR (6th)，研究發現 0.025 % Voco Solobond M (5th) 能誘導 COX-2 蛋白表現 ， 但 Voco Futurabond NR (6th) 則否 。 為了模擬此兩種牙本質黏著劑中 ， 成分所佔的百分比 ， 並去了解不同濃度的 HEMA 是否會影響 BisGMA 對 COX-2 蛋白的誘導表現 。 本研究選擇 0.33 mM - 0.99 mM HEMA 共同處理 30μM BisGMA ， 發現不會影響 BisGMA 所誘導的 COX-2 蛋白表現 。 此結果指出 Voco Futurabond NR (6th) 不能誘導 COX-2 蛋白表現和 HEMA 無關 。 綜合以上結果得知 ， 牙本質黏著劑中不同的成分 ， 會對不同類型的發炎相關蛋白 ， 造成不同影響 ， 並且能影響這些蛋白的轉錄和轉譯作用 。 本研究提出了 BisGMA 對 HUVECs 的 COX-2 蛋白表現的作用和可能機制 ， 並且也探討了 HEMA 對 HUVECs 的作用 ； 所有的研究成果，提供了牙本質黏著劑對靜脈內皮細胞中發炎作用的可能方向。 | zh_TW |
| dc.description.abstract | Dentin bonding agents are broadly used for clinical dental therapy, like dental caries. Dental caries primarily caused by dental plaque, which can induce gingival inflammation. In previous research, dental plaque can induce proinflammatory mediators like tumor necrosis factor alpha ( TNF-α). TNF-α is a well known inducer which can induce inflammatory-associated proteins like intracellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and cyclooxygenase-2 (COX-2) in endothelial cells . Thus, the periodontal tissues under the situation of dental caries may often be inflammatory. Dentin bonding agents should be stable in the oral environment, but some components may release from adhesive materials and composite resin even after polymerization. Besides, some data have shown some composite bonding agents have an acute vasodilating effect on the dental pulp. The majore components leached from dentin bonding agents are monomers, like bisphenol-glycidylmethacrylate (BisGMA) and 2-hydroxyethyl methacrylate (HEMA). There are many researches about toxicity of monomers but the effects of monomers to circulation are still not clear. Thus, we want to know the effect and mechanisms of monomer components on inflammation in vein endothelial cells. In this work, we studied inflammation-associated proteins, ICAM-1, VCAM-1 and COX-2. Primary-cultured-HUVECs (human umbilical vein endothelial cells) are used for this research. Reverse transcriptase PCR (RT-PCR) and western blotting analysis are used for this investigation to find the effects and mechanisms of BisGMA on ICAM-1,VCAM-1 and COX-2 in HUVECs.
First, we find the induction of 30μM BisGMA on COX-2 in HUVECs, but no effects on ICAM-1 and VCAM-1 in HUVECs. Thus, we check COX-2 mRNA and also see the induction by BisGMA. Further, we first find two pathways of BisGMA-induced COX-2 by western blotting analysis. One is through Epidermal growth factor receptor (EGFR) to Akt, and the other is though p38. Second, to detect the effects of HEMA on inflammatory-associated proteins in HUVECs, we find there are no effects of HEMA on ICAM-1, VCAM-1 and COX-2. However, pretreat HEMA then cotreat with TNF-α. we first find 0.99mM HEMA can inhibit TNF-α-induced ICAM-1, VCAM-1 and COX-2. This results show 0.99 mM may inhibit inflammation. Third, we compare the effects of monomers and mixture, dentin bonding agents on inflammatory-associated proteins. We find 0.025 % Voco Solobond M (5th) can induce COX-2 but Voco Futurabond NR (6th) can’t. To imitate the possible percentage of components in these two dentin bonding agents and understand whether concentration of HEMA can affect the induction of BisGMA on COX-2, we select 0.33 mM - 0.99 mM HEMA cotreat with 30μM BisGMA and still see the induction of COX-2. This results point that the reason of Voco Futurabond NR (6th) can’t induce COX-2 expression is not HEMA. Together, these results indicated that the different compositions of dentin bonding agents may cause different effects on different types of inflammatory-associated proteins and meanwhile may affect transcription and translation of these proteins. This research shows the possible mechanisms of BisGMA on COX-2 in HUVECs and detects some effects of HEMA in HUVECs. All of these provide a possible direction of dentin bonding agents on inflammation in vein endothelial cells. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-15T04:16:28Z (GMT). No. of bitstreams: 1 ntu-98-R96447001-1.pdf: 7386452 bytes, checksum: 3540376c386c651954eb613c0ebec689 (MD5) Previous issue date: 2009 | en |
| dc.description.tableofcontents | 口試委員會審定書 p.i
謝誌 p.ii 中文摘要 p.iii 英文摘要 p.v 目錄 p.vii 縮寫表(Abbreviations) p.x 圖表目錄(Figures and Tables) p.xi 第一章 緒論 (Introduction) p.2 第二章 實驗材料與方法 (Materials and Methods) p.21 第三章 實驗結果(Results) p.29 第四章 討論(Discussion) p.41 第五章 結論(Conclusion) p.52 參考文獻(References) p.54 圖表集(Figures and Tables) p.69 | |
| dc.language.iso | zh-TW | |
| dc.subject | 人類靜脈內皮細胞 | zh_TW |
| dc.subject | 環氧化酶 | zh_TW |
| dc.subject | 牙本質黏著劑 | zh_TW |
| dc.subject | 細胞黏著分子 | zh_TW |
| dc.subject | 單體 | zh_TW |
| dc.subject | 發炎 | zh_TW |
| dc.subject | denting bonding agents | en |
| dc.subject | cyclooxygenase-2 | en |
| dc.subject | cell adhesion molecule | en |
| dc.subject | inflammation | en |
| dc.subject | HUVE Cs | en |
| dc.subject | monomer | en |
| dc.title | 牙本質黏著劑之單體對人類靜脈內皮細胞發炎反應的作用和機制 | zh_TW |
| dc.title | The Effects and Mechanisms of Monomers in Dentin Bonding Agents on inflammation in Human Umbilical Vein Endothelial Cells | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 98-1 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 康照洲,彭福佐,鄭景暉 | |
| dc.subject.keyword | 牙本質黏著劑,單體,人類靜脈內皮細胞,發炎,細胞黏著分子,環氧化酶,-2, | zh_TW |
| dc.subject.keyword | denting bonding agents,monomer,HUVE Cs,inflammation,cell adhesion molecule,cyclooxygenase-2, | en |
| dc.relation.page | 91 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2010-01-03 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 毒理學研究所 | zh_TW |
| 顯示於系所單位： | 毒理學研究所 | |
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