請用此 Handle URI 來引用此文件：
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/55746完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 曾琬瑜(Wan-Yu Tseng) | |
| dc.contributor.author | Yu-Jen Hu | en |
| dc.contributor.author | 胡裕仁 | zh_TW |
| dc.date.accessioned | 2021-06-16T05:07:58Z | - |
| dc.date.available | 2014-10-15 | |
| dc.date.copyright | 2014-10-15 | |
| dc.date.issued | 2014 | |
| dc.date.submitted | 2014-08-20 | |
| dc.identifier.citation | 1. Cramer, N.B., J.W. Stansbury, and C.N. Bowman, Recent advances and developments in composite dental restorative materials. J Dent Res, 2011. 90(4): p. 402-16.
2. Ferracane, J.L., Resin composite--state of the art. Dent Mater, 2011. 27(1): p. 29-38. 3. Williams, D.F., On the nature of biomaterials. Biomaterials, 2009. 30(30): p. 5897-909. 4. Buonocore, M.G., A simple method of increasing the adhesion of acrylic filling materials to enamel surfaces. J Dent Res, 1955. 34(6): p. 849-53. 5. Gilpatrick, R.O., J.A. Ross, and R.J. Simonsen, Resin-to-enamel bond strengths with various etching times. Quintessence Int, 1991. 22(1): p. 47-9. 6. Gwinnett, A.J. and J.A. Kanca, 3rd, Micromorphology of the bonded dentin interface and its relationship to bond strength. Am J Dent, 1992. 5(2): p. 73-7. 7. Shaffer, S.E., W.W. Barkmeier, and W.P. Kelsey, 3rd, Effects of reduced acid conditioning time on enamel microleakage. Gen Dent, 1987. 35(4): p. 278-80. 8. Harald O. Heymann, E.J.S., Jr. , Addre V. Ritter, Sturdevant's Art and Science of Operative Dentistry. 6th ed. 2013: MOSBY. 9. McLean JW, K., IRH: A clinical and pathological evaluation of a sulfinic acid activated resin for use in restorative dentistry. Br Dent J, 1952(93): p. 255-69. 10. Buonocore M, W.W., Brudevold F, A report on a resin composition capable of bonding to human dentin surfaces. J Dent Res, 1956(35): p. 846-51. 11. Nakabayashi, N. and K. Takarada, Effect of HEMA on bonding to dentin. Dent Mater, 1992. 8(2): p. 125-30. 12. Jacobsan T, M.R., Soderholm KJ., Dentin bonding through interpenetrating network formation. Transactions of the Academy of Dental Materials, 1994. 7: p. 45-52. 13. Fong, D.-W. and E. Grunwald, Acid dissociation in acetone-water mixtures. An anomalous medium effect when London dispersion forces are large. The Journal of Physical Chemistry, 1969. 73(11): p. 3909-3911. 14. Mohan, B. and D. Kandaswamy, A confocal microscopic evaluation of resin-dentin interface using adhesive systems with three different solvents bonded to dry and moist dentinan in vitro study. Quintessence Int, 2005. 36(7-8): p. 511-21. 15. Abate, P.F., V.I. Rodriguez, and R.L. Macchi, Evaporation of solvent in one-bottle adhesives. J Dent, 2000. 28(6): p. 437-40. 16. Pashley, D.H., et al., Solvent-induced dimensional changes in EDTA-demineralized dentin matrix. J Biomed Mater Res, 2001. 56(2): p. 273-81. 17. El Feninat, F., et al., A tapping mode AFM study of collapse and denaturation in dentinal collagen. Dent Mater, 2001. 17(4): p. 284-8. 18. Perdigao, J., E.J. Swift, Jr., and G.C. Lopes, Effects of repeated use on bond strengths of one-bottle adhesives. Quintessence Int, 1999. 30(12): p. 819-23. 19. Moszner, N., U. Salz, and J. Zimmermann, Chemical aspects of self-etching enamel-dentin adhesives: a systematic review. Dent Mater, 2005. 21(10): p. 895-910. 20. Imazato, S., et al., Degree of conversion of composites measured by DTA and FTIR. Dent Mater, 2001. 17(2): p. 178-83. 21. Van Meerbeek, B., et al., Buonocore memorial lecture. Adhesion to enamel and dentin: current status and future challenges. Oper Dent, 2003. 28(3): p. 215-35. 22. Spencer, P., et al., Interfacial chemistry of the dentin/adhesive bond. J Dent Res, 2000. 79(7): p. 1458-63. 23. Miyazaki, M., H. Onose, and B.K. Moore, Analysis of the dentin-resin interface by use of laser Raman spectroscopy. Dent Mater, 2002. 18(8): p. 576-80. 24. Sano, H., et al., Microporous dentin zone beneath resin-impregnated layer. Oper Dent, 1994. 19(2): p. 59-64. 25. John W Farah, J.M.P., Update:Self bonding agents. The Dental Advisor, 2004. 21(8). 26. Jacobsen, T. and K.J. Soderholm, Some effects of water on dentin bonding. Dent Mater, 1995. 11(2): p. 132-6. 27. Gregoire, G.L., B.A. Akon, and A. Millas, Interfacial micromorphological differences in hybrid layer formation between water- and solvent-based dentin bonding systems. J Prosthet Dent, 2002. 87(6): p. 633-41. 28. Perdigao, J., et al., Enamel bond strengths of pairs of adhesives from the same manufacturer. Oper Dent, 2005. 30(4): p. 492-9. 29. Salz, U., et al., Hydrolytic stability of self-etching adhesive systems. J Adhes Dent, 2005. 7(2): p. 107-16. 30. Pashley, D.H., et al., The microtensile bond test: a review. J Adhes Dent, 1999. 1(4): p. 299-309. 31. Inoue, S., et al., Microtensile bond strength of eleven contemporary adhesives to enamel. Am J Dent, 2003. 16(5): p. 329-34. 32. Peutzfeldt, A., Resin composites in dentistry: the monomer systems. Eur J Oral Sci, 1997. 105(2): p. 97-116. 33. Van Landuyt, K.L., et al., Systematic review of the chemical composition of contemporary dental adhesives. Biomaterials, 2007. 28(26): p. 3757-85. 34. Durner, J., et al., Eluted substances from unpolymerized and polymerized dental restorative materials and their Nernst partition coefficient. Dent Mater, 2010. 26(1): p. 91-9. 35. Ferracane, J.L., Elution of leachable components from composites. J Oral Rehabil, 1994. 21(4): p. 441-52. 36. Santerre, J.P., L. Shajii, and B.W. Leung, Relation of dental composite formulations to their degradation and the release of hydrolyzed polymeric-resin-derived products. Crit Rev Oral Biol Med, 2001. 12(2): p. 136-51. 37. Drummond, J.L., Degradation, fatigue, and failure of resin dental composite materials. J Dent Res, 2008. 87(8): p. 710-9. 38. Ferracane, J.L., Resin-based composite performance: are there some things we can't predict? Dent Mater, 2013. 29(1): p. 51-8. 39. Meryon, S.D. and A.M. Brook, In vitro cytotoxicity of three dentine bonding agents. J Dent, 1989. 17(6): p. 279-83. 40. Bouillaguet, S., et al., The influence of dentine permeability on cytotoxicity of four dentine bonding systems, in vitro. J Oral Rehabil, 1998. 25(1): p. 45-51. 41. Hashieh, I.A., et al., In vitro cytotoxicity of one-step dentin bonding systems. J Endod, 1999. 25(2): p. 89-92. 42. Chen, R.S., et al., Cytotoxicity of three dentin bonding agents on human dental pulp cells. J Dent, 2003. 31(3): p. 223-9. 43. Grobler, S.R., et al., Cytotoxicity of two concentrations of a dentine bonding agent on mouse 3T3 and human pulp fibroblast cell-lines. Sadj, 2004. 59(9): p. 368-70, 372. 44. Moodley, D., S.R. Grobler, and A. Olivler, Cytotoxicity of a dentine bonding agent on four different cell-lines. Sadj, 2005. 60(6): p. 234-6. 45. Mirmotalebi, F. and S. Nazari, Comparison of cytotoxicity of three dentin bonding systems with two thicknesses of dentin barrier on l929 cell line. Iran Endod J, 2006. 1(3): p. 109-13. 46. Prica, D., et al., Genotoxicity evaluation of five different dentin bonding agents by chromosomal aberration analysis. J Oral Rehabil, 2006. 33(6): p. 462-71. 47. Yasuda, Y., et al., Cytotoxicity of one-step dentin-bonding agents toward dental pulp and odontoblast-like cells. J Oral Rehabil, 2008. 35(12): p. 940-6. 48. Sengun, A., et al., Cytotoxicity evaluation of dentin bonding agents by dentin barrier test on 3-dimensional pulp cells. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 2011. 112(3): p. e83-8. 49. Kierklo, A., et al., Cytotoxicity evaluation of three light-cured dentin adhesive materials on human gingival fibroblasts, ex vivo. Adv Med Sci, 2012. 57(2): p. 385-90. 50. Van Landuyt, K.L., et al., How much do resin-based dental materials release? A meta-analytical approach. Dent Mater, 2011. 27(8): p. 723-47. 51. Seiss, M., et al., Quantitative determination of TEGDMA, BHT, and DMABEE in eluates from polymerized resin-based dental restorative materials by use of GC/MS. Arch Toxicol, 2009. 83(12): p. 1109-15. 52. Costa, C.A., J. Hebling, and C.T. Hanks, Current status of pulp capping with dentin adhesive systems: a review. Dent Mater, 2000. 16(3): p. 188-97. 53. Murray, P.E., et al., Comparison of pulp responses following restoration of exposed and non-exposed cavities. J Dent, 2002. 30(5-6): p. 213-22. 54. Modena, K.C., et al., Cytotoxicity and biocompatibility of direct and indirect pulp capping materials. J Appl Oral Sci, 2009. 17(6): p. 544-54. 55. Hanks, C.T., et al., Cytotoxic effects of resin components on cultured mammalian fibroblasts. J Dent Res, 1991. 70(11): p. 1450-5. 56. Geurtsen, W., Biocompatibility of resin-modified filling materials. Crit Rev Oral Biol Med, 2000. 11(3): p. 333-55. 57. Nocca, G., et al., Identification of glutathione-methacrylates adducts in gingival fibroblasts and erythrocytes by HPLC-MS and capillary electrophoresis. Dent Mater, 2011. 27(5): p. e87-98. 58. Schweikl, H., G. Spagnuolo, and G. Schmalz, Genetic and cellular toxicology of dental resin monomers. J Dent Res, 2006. 85(10): p. 870-7. 59. Chang, H.H., et al., Stimulation of glutathione depletion, ROS production and cell cycle arrest of dental pulp cells and gingival epithelial cells by HEMA. Biomaterials, 2005. 26(7): p. 745-53. 60. Schweikl, H., et al., Inhibition of TEGDMA and HEMA-induced genotoxicity and cell cycle arrest by N-acetylcysteine. Dent Mater, 2007. 23(6): p. 688-95. 61. Eckhardt, A., et al., Inhibition of cytokine and surface antigen expression in LPS-stimulated murine macrophages by triethylene glycol dimethacrylate. Biomaterials, 2009. 30(9): p. 1665-74. 62. Schmalz, G., S. Krifka, and H. Schweikl, Toll-like receptors, LPS, and dental monomers. Adv Dent Res, 2011. 23(3): p. 302-6. 63. Bolling, A.K., et al., Dental monomers inhibit LPS-induced cytokine release from the macrophage cell line RAW264.7. Toxicol Lett, 2013. 216(2-3): p. 130-8. 64. Tsukimura, N., et al., N-acetyl cysteine (NAC)-mediated detoxification and functionalization of poly(methyl methacrylate) bone cement. Biomaterials, 2009. 30(20): p. 3378-89. 65. Galler, K.M., et al., TEGDMA reduces mineralization in dental pulp cells. J Dent Res, 2011. 90(2): p. 257-62. 66. About, I., Dentin regeneration in vitro: the pivotal role of supportive cells. Adv Dent Res, 2011. 23(3): p. 320-4. 67. Bakopoulou, A., et al., Effects of HEMA and TEDGMA on the in vitro odontogenic differentiation potential of human pulp stem/progenitor cells derived from deciduous teeth. Dent Mater, 2011. 27(6): p. 608-17. 68. Bakopoulou, A., et al., Effects of resinous monomers on the odontogenic differentiation and mineralization potential of highly proliferative and clonogenic cultured apical papilla stem cells. Dent Mater, 2012. 28(3): p. 327-39. 69. Montheard, J.-P., M. Chatzopoulos, and D. Chappard, 2-Hydroxyethyl Methacrylate (HEMA): Chemical Properties and Applications in Biomedical Fields. Journal of Macromolecular Science, Part C, 1992. 32(1): p. 1-34. 70. Jontell, M., et al., Effects of unpolymerized resin components on the function of accessory cells derived from the rat incisor pulp. J Dent Res, 1995. 74(5): p. 1162-7. 71. Sandberg, E., et al., HEMA bound to self-protein promotes auto-antibody production in mice. J Dent Res, 2002. 81(9): p. 633-6. 72. Paranjpe, A., et al., Resin monomer 2-hydroxyethyl methacrylate (HEMA) is a potent inducer of apoptotic cell death in human and mouse cells. J Dent Res, 2005. 84(2): p. 172-7. 73. Jewett, A., et al., Differential secretion of TNF-alpha and IFN-gamma by human peripheral blood-derived NK subsets and association with functional maturation. J Clin Immunol, 1996. 16(1): p. 46-54. 74. Jewett, A., M. Cavalcanti, and B. Bonavida, Pivotal role of endogenous TNF-alpha in the induction of functional inactivation and apoptosis in NK cells. J Immunol, 1997. 159(10): p. 4815-22. 75. About, I., et al., Influence of resinous monomers on the differentiation in vitro of human pulp cells into odontoblasts. J Biomed Mater Res, 2002. 63(4): p. 418-23. 76. Droge, W., Free radicals in the physiological control of cell function. Physiol Rev, 2002. 82(1): p. 47-95. 77. Kohen, R. and A. Nyska, Oxidation of biological systems: oxidative stress phenomena, antioxidants, redox reactions, and methods for their quantification. Toxicol Pathol, 2002. 30(6): p. 620-50. 78. Genestra, M., Oxyl radicals, redox-sensitive signalling cascades and antioxidants. Cell Signal, 2007. 19(9): p. 1807-19. 79. Forman, H.J. and M. Torres, Redox signaling in macrophages. Mol Aspects Med, 2001. 22(4-5): p. 189-216. 80. Valko, M., et al., Role of oxygen radicals in DNA damage and cancer incidence. Mol Cell Biochem, 2004. 266(1-2): p. 37-56. 81. Pervaiz, S., R. Taneja, and S. Ghaffari, Oxidative stress regulation of stem and progenitor cells. Antioxid Redox Signal, 2009. 11(11): p. 2777-89. 82. D'Autreaux, B. and M.B. Toledano, ROS as signalling molecules: mechanisms that generate specificity in ROS homeostasis. Nat Rev Mol Cell Biol, 2007. 8(10): p. 813-24. 83. Halliwell, B., Antioxidant defence mechanisms: from the beginning to the end (of the beginning). Free Radic Res, 1999. 31(4): p. 261-72. 84. Trachootham, D., et al., Redox regulation of cell survival. Antioxid Redox Signal, 2008. 10(8): p. 1343-74. 85. Circu, M.L. and T.Y. Aw, Reactive oxygen species, cellular redox systems, and apoptosis. Free Radic Biol Med, 2010. 48(6): p. 749-62. 86. Forman, H.J., H. Zhang, and A. Rinna, Glutathione: overview of its protective roles, measurement, and biosynthesis. Mol Aspects Med, 2009. 30(1-2): p. 1-12. 87. Lu, S.C., Regulation of glutathione synthesis. Mol Aspects Med, 2009. 30(1-2): p. 42-59. 88. Han, D., et al., Mechanisms of liver injury. III. Role of glutathione redox status in liver injury. Am J Physiol Gastrointest Liver Physiol, 2006. 291(1): p. G1-7. 89. Schafer, F.Q. and G.R. Buettner, Redox environment of the cell as viewed through the redox state of the glutathione disulfide/glutathione couple. Free Radic Biol Med, 2001. 30(11): p. 1191-212. 90. Jones, D.P., Redefining oxidative stress. Antioxid Redox Signal, 2006. 8(9-10): p. 1865-79. 91. Stanislawski, L., et al., TEGDMA-induced toxicity in human fibroblasts is associated with early and drastic glutathione depletion with subsequent production of oxygen reactive species. J Biomed Mater Res A, 2003. 66(3): p. 476-82. 92. Walther, U.I., et al., Antioxidative vitamins decrease cytotoxicity of HEMA and TEGDMA in cultured cell lines. Arch Oral Biol, 2004. 49(2): p. 125-31. 93. Samuelsen, J.T., et al., Role of thiol-complex formation in 2-hydroxyethyl- methacrylate-induced toxicity in vitro. J Biomed Mater Res A, 2011. 96(2): p. 395-401. 94. Schweikl, H. and G. Schmalz, Triethylene glycol dimethacrylate induces large deletions in the hprt gene of V79 cells. Mutat Res, 1999. 438(1): p. 71-8. 95. Geurtsen, W. and G. Leyhausen, Chemical-Biological Interactions of the resin monomer triethyleneglycol-dimethacrylate (TEGDMA). J Dent Res, 2001. 80(12): p. 2046-50. 96. Yamada, M., et al., N-acetyl cysteine (NAC)-assisted detoxification of PMMA resin. J Dent Res, 2008. 87(4): p. 372-7. 97. Yamada, M. and T. Ogawa, Chemodynamics underlying N-acetyl cysteine-mediated bone cement monomer detoxification. Acta Biomater, 2009. 5(8): p. 2963-73. 98. Nocca, G., et al., N-acetyl cysteine directed detoxification of 2-hydroxyethyl methacrylate by adduct formation. Biomaterials, 2010. 31(9): p. 2508-16. 99. Zafarullah, M., et al., Molecular mechanisms of N-acetylcysteine actions. Cell Mol Life Sci, 2003. 60(1): p. 6-20. 100. Paranjpe, A., et al., N-acetylcysteine protects dental pulp stromal cells from HEMA-induced apoptosis by inducing differentiation of the cells. Free Radic Biol Med, 2007. 43(10): p. 1394-408. 101. Paranjpe, A., et al., N-acetyl cysteine mediates protection from 2-hydroxyethyl methacrylate induced apoptosis via nuclear factor kappa B-dependent and independent pathways: potential involvement of JNK. Toxicol Sci, 2009. 108(2): p. 356-66. 102. Baeuerle, P.A. and T. Henkel, Function and activation of NF-kappa B in the immune system. Annu Rev Immunol, 1994. 12: p. 141-79. 103. Beg, A.A. and D. Baltimore, An essential role for NF-kappaB in preventing TNF-alpha-induced cell death. Science, 1996. 274(5288): p. 782-4. 104. Wang, C.Y., M.W. Mayo, and A.S. Baldwin, Jr., TNF- and cancer therapy-induced apoptosis: potentiation by inhibition of NF-kappaB. Science, 1996. 274(5288): p. 784-7. 105. Van Antwerp, D.J., et al., Suppression of TNF-alpha-induced apoptosis by NF-kappaB. Science, 1996. 274(5288): p. 787-9. 106. Baichwal, V.R. and P.A. Baeuerle, Activate NF-kappa B or die? Curr Biol, 1997. 7(2): p. R94-6. 107. Van de Water, B., M. Kruidering, and J.F. Nagelkerke, F-actin disorganization in apoptotic cell death of cultured rat renal proximal tubular cells. Vol. 270. 1996. F593-F603. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/55746 | - |
| dc.description.abstract | 中文摘要
聚合黏著系統及光聚合樹脂大量的使用於臨床工作之中，但常發現有些病人在使用這些材料填補齲齒後，發生術後敏感甚至是牙髓發炎的現象。黏著系統中所使用的單體是否具有毒性，長久以來，已是備受爭議的問題。一般認為樹脂單體在到達一定濃度後具有細胞毒性，但是這類單體對細胞影響的作用機轉尚未曾明朗。 本實驗目的在於研究牙科黏著系統中最常見的甲基丙烯酸羥基乙酯（2-Hydroxyethyl Methacrylate，HEMA）對於人類嬰兒牙髓細胞(Human baby dental pulp cell，HDPC)及小鼠胸腺纖維母細胞株(NIH/3T3)所造成的影響。本實驗測試使用半數中毒濃度(median toxic concentration，TC50)以下單體濃度培養細胞後，細胞在短期(24hr)、中期(72hr)，長期(120hr)的細胞反應。首先先以細胞存活率分析((3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) MTT assay)測試HEMA對兩種細胞在24小時，72小時，以及120小時的TC50，分別約為HDPC:24小時10mM、72小時4mM 、120小時2.4mM；以及3T3 24小時7.4mM、72小時3.2mM、120小時2.67mM。 之後以0mM(未加單體)、0.25mM、1mM、2.5mM、5mM，以及10mM濃度培養上述兩種細胞24小時後，觀察細胞存活狀況；中期(72hr)以及長期(120hr) 的培養濃度分別為0mM、0.125mM、0.25mM、1mM、2mM、4mM。同時，在光學顯微鏡下觀察HEMA單體對細胞形態結構上所造成的改變。本實驗更進一步利用流式細胞儀(flow cytometry)以及Annexin V/PI雙染法測量經過HEMA單體處理後，HDPC以及3T3所引起的細胞死亡模式。之後，為了針對臨床治療效果，進行更深入的研究，我們將實驗集中於人類嬰兒牙髓細胞。 本實驗為了探討HEMA對人類牙髓細胞穀胱甘肽(Glutathione,GSH)系統的影響，利用測定GSSG/GSH的方式來檢驗細胞中的GSH是否真的被HEMA單體所產生的氧化壓力(oxidative stress)消耗。結果證實，對照控制組，接觸HEMA濃度越高則GSH消耗的越多。另外為了解其觸發的信息路徑，也利用免疫酵素連結測試(ELISA)測定磷酸化的NF-ĸB(phosphor NF-ĸB)與全體NF-ĸB(total NF-ĸB)，以確認NF-ĸB是否在HEMA單體觸發牙髓細胞進入凋亡的信息傳遞中扮演重要的角色；實驗中發現，在短期（24hr，72hr）接觸的情況下，磷酸化NF-ĸB的量與細胞凋亡的比率成現相反的趨勢意味著NF-ĸB可能能夠保護細胞避免凋亡，而在五天的實驗觀察發現磷酸化NF-ĸB隨著細胞凋亡比率上升而上升，或許意味著NF-ĸB在長期接觸下導致細胞走向凋亡。 關鍵詞： 甲基丙烯酸羥基乙酯、牙髓細胞、毒性、黏著系統、單體、穀胱甘肽 | zh_TW |
| dc.description.abstract | Abstract
Dentin bonding system (DBS) was first introduced about over 50 years ago. Nowadays, it becomes more and more popular and necessary in dental practice. It provides aesthetic and strong bonding strength between tooth structure and restorations. Some studies revealed the chemical component in DBS such as monomers may irritate the pulp complex lead to pulp in-flammation and post-operative hypersensitivity. Evidences showed chemical monomers at certain concentrations is cytotoxic , and might cause cell apoptosis. Although the detail mechanism is unclear, several hypotheses have been proposed. This study will focus one of the most common monomer used in DBS: 2-Hydroxyethyl Methacrylate (HEMA). Frist, the MTT assay was taken to determine the concentrations of TC50 of NIH/NIH/3T3 cell line and HDPC on HEMA. The results of TC50 of HEMA to HDPC at 24hrs is about 10mM, 72hrs is 4mM, and 120hrs is 2.4mM ; TC50 of HEMA to NIH/3T3 cell is about 7.4mM, 72hrs is 3.2mM, and 120hrs is 2.67mM. Then, the lower concentration (for 24hrs test: 0mM, 0.25mM, 1mM, 2.5mM, 5mM, and 10mM ; for 72hrs and 120 hrs : 0mM, 0.125mM, 0.25mM, 1mM, 2mM, and 4mM) was used in cell culture and analyzed with MTT assay. Also, to observe the changes of cell morphology of HEMA-treated cells, the photos were taken under light microscope 200x. Moreover, in or-der to investigate the pattern of cell death, the FITC-Annexin V/PI Dual staining was carried out on HDPC and NIH/3T3 cells , under all concentration of HEMA monomer which are mentioned before. This study also used fluorescent staining technique to enhance cell skeleton by Phalloidin stain and cell DNA was stained by using Hoechst stains in order to observe cell morphology changing and apoptotic bodies. And then we focus on HPDC cell use GSSG/GSH ELISA test and NF-ĸB p65 (to-tal/phosph) assay hopefully to obtain further information of HEMA induced ROS increases and GSH depletion and activate NF-ĸB signal pathway. The initial result indicated that in HEMA induced cell apoptosis, cell apoptosis rate rise with GSH depletion, and for phosphor NF-ĸB, in short term (<72hr), NF-ĸB may protect cell from HEMA induced apoptosis; in long term (120hr), NF-ĸB may lead cell to apoptosis in-duced by HEMA. Key words: monomer, HEMA, HDPC, cytotoxicity, GSH, NF-κB | en |
| dc.description.provenance | Made available in DSpace on 2021-06-16T05:07:58Z (GMT). No. of bitstreams: 1 ntu-103-R00422003-1.pdf: 8499811 bytes, checksum: d5906ba30785f5721ce24577f0e4dbfb (MD5) Previous issue date: 2014 | en |
| dc.description.tableofcontents | 口試委員審定書……………………………………………………………………………….I
誌謝……………………………………………………………………………………………II 中文摘要……………………………………………………………………………………...III Abstract………………………………………………………………………………………..V 目錄………………………………………………………………………………………….VII 圖目錄………………………………………………………………………………………..IX 一、 前言 1 二、研究特定目標 1 三、文獻回顧 2 3.1牙齒黏著技術的演進: 2 3.2牙釉質與牙本質的表面差異 3 3.3牙本質黏著系統發展與演進 4 3.3.1全酸蝕系統 5 3.3.2自酸蝕系統(self-etching system) 8 3.4牙本質黏著劑中常使用的單體: 9 3.5牙本質黏著劑毒性研究 10 3.6單體的毒性研究 10 3.7 HEMA對細胞的影響: 12 3.7.1活性氧理論 13 3.8細胞凋亡 16 3.9 NF-ĸB在細胞中所扮演的角色 16 四、實驗動機與假設 18 五、實驗材料與方法: 18 5.1材料： 18 5.2儀器： 18 5.3細胞培養： 19 細胞株實驗小鼠纖維母細胞株(NIH/NIH/3T3) 19 人類牙髓細胞(Human dental pulp Cells ；HDPC) 19 5.4光學顯微鏡下細胞分析 20 5.5細胞存活率分析(MTT assay) 20 5.6 Annexin V/PI staining 20 5.6.1基本原理 21 5.6.2試劑以及儀器 21 5.6.3實驗步骤： 21 5.6.4结果判斷： 22 5.7螢光顯微鏡: 23 5.7.1螢光顯微鏡基本原理 23 5.7.2肌動蛋白絲(F-actin)染色: 24 5.7.3赫斯特染色法 24 5.8 GSH/GSSG測定 25 5.8.1材料: 25 5.8.2方法: 25 5.9 NF-ĸB測定All in one well protocol 26 5.10 統計方法 27 六、實驗結果: 27 6.1 MTT assay細胞存活率分析實驗: 27 6.2光學顯微鏡觀察結果 28 6.3流式細胞儀Annexin V/PI染色分析 29 6.4.螢光顯微鏡觀察細胞形態變化(F-actin 以及赫斯特染色): 31 6.5穀胱甘肽GSH免疫分析： 31 6.6磷酸化NF-ĸB測定 32 七、討論: 33 八、結論: 37 參考文獻 81 | |
| dc.language.iso | zh-TW | |
| dc.title | 甲基丙烯酸羥乙酯單體的毒性研究與分析 | zh_TW |
| dc.title | The mechanism of HEMA cytotoxicity | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 102-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 林立德(Li-Deh Lin),洪志遠(Chi-Yuan Hong) | |
| dc.subject.keyword | 單體,毒性,甲基丙烯酸羥乙酯,穀胱胺?,牙髓細胞,黏著細胞, | zh_TW |
| dc.subject.keyword | monomer,HEMA,HDPC,cytotocicity,GSH,NF-κB, | en |
| dc.relation.page | 87 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2014-08-20 | |
| dc.contributor.author-college | 牙醫專業學院 | zh_TW |
| dc.contributor.author-dept | 臨床牙醫學研究所 | zh_TW |
| 顯示於系所單位： | 臨床牙醫學研究所 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-103-1.pdf 目前未授權公開取用 | 8.3 MB | Adobe PDF |
系統中的文件，除了特別指名其著作權條款之外，均受到著作權保護，並且保留所有的權利。