請用此 Handle URI 來引用此文件:
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/42804
完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 盧國賢 | |
dc.contributor.author | Shih-Chen Fu | en |
dc.contributor.author | 傅詩宸 | zh_TW |
dc.date.accessioned | 2021-06-15T01:24:06Z | - |
dc.date.available | 2014-09-15 | |
dc.date.copyright | 2009-09-15 | |
dc.date.issued | 2009 | |
dc.date.submitted | 2009-07-23 | |
dc.identifier.citation | Arenas, P. 1987. Medicine and magic among the Maka Indians of the Paraguayan Chaco. J Ethnopharmacol. 21:279-95.
Bastien, J.W. 1983. Pharmacopeia of Qollahuaya Andeans. J Ethnopharmacol. 8:97-111. Beanes, S.R., C. Dang, C. Soo, and K. Ting. 2003. Skin repair and scar formation: the central role of TGF-beta. Expert Rev Mol Med. 5:1-22. Camp, D.F., A. Ateaque, and W.A. Dickson. 2003. Cryogenic burns from aerosol sprays: a report of two cases and review of the literature. Br J Plast Surg. 56:815-7. Chen, G., and D.V. Goeddel. 2002. TNF-R1 signaling: a beautiful pathway. Science. 296:1634-5. Chen, R.N., G.M. Wang, C.H. Chen, H.O. Ho, and M.T. Sheu. 2006. Development of N,O-(carboxymethyl)chitosan/collagen matrixes as a wound dressing. Biomacromolecules. 7:1058-64. Dobreva, I., G. Waeber, R.W. James, and C. Widmann. 2006. Interleukin-8 secretion by fibroblasts induced by low density lipoproteins is p38 MAPK-dependent and leads to cell spreading and wound closure. J Biol Chem. 281:199-205. Fahey, T.J., 3rd, B. Sherry, K.J. Tracey, S. van Deventer, W.G. Jones, 2nd, J.P. Minei, S. Morgello, G.T. Shires, and A. Cerami. 1990. Cytokine production in a model of wound healing: the appearance of MIP-1, MIP-2, cachectin/TNF and IL-1. Cytokine. 2:92-9. Fallon, J.H., K.B. Seroogy, S.E. Loughlin, R.S. Morrison, R.A. Bradshaw, D.J. Knaver, and D.D. Cunningham. 1984. Epidermal growth factor immunoreactive material in the central nervous system: location and development. Science. 224:1107-9. Gillitzer, R., and M. Goebeler. 2001. Chemokines in cutaneous wound healing. J Leukoc Biol. 69:513-21. Goncalves, A.M., M.E. Vasconcellos, R. Docampo, F.S. Cruz, W. de Souza, and W. Leon. 1980. Evaluation of the toxicity of 3-allyl-beta-lapachone against Trypanosoma cruzi bloodstream forms. Mol Biochem Parasitol. 1:167-76. Guiraud, P., R. Steiman, G.M. Campos-Takaki, F. Seigle-Murandi, and M. Simeon de Buochberg. 1994. Comparison of antibacterial and antifungal activities of lapachol and beta-lapachone. Planta Med. 60:373-4. Henry, G., and W.L. Garner. 2003. Inflammatory mediators in wound healing. Surg Clin North Am. 83:483-507. Herbst, R.S. 2004. Review of epidermal growth factor receptor biology. Int J Radiat Oncol Biol Phys. 59:21-6. Klagsbrun, M., and P.A. D'Amore. 1996. Vascular endothelial growth factor and its receptors. Cytokine Growth Factor Rev. 7:259-70. Kung, H.N., M.J. Yang, C.F. Chang, Y.P. Chau, and K.S. Lu. 2008. In vitro and in vivo wound healing-promoting activities of beta-lapachone. Am J Physiol Cell Physiol. 295:C931-43. Li, C.J., L. Averboukh, and A.B. Pardee. 1993. beta-Lapachone, a novel DNA topoisomerase I inhibitor with a mode of action different from camptothecin. J Biol Chem. 268:22463-8. Li, C.J., C. Wang, and A.B. Pardee. 1995. Induction of apoptosis by beta-lapachone in human prostate cancer cells. Cancer Res. 55:3712-5. Li, Y.Z., C.J. Li, A.V. Pinto, and A.B. Pardee. 1999. Release of mitochondrial cytochrome C in both apoptosis and necrosis induced by beta-lapachone in human carcinoma cells. Mol Med. 5:232-9. Manna, S.K., Y.P. Gad, A. Mukhopadhyay, and B.B. Aggarwal. 1999. Suppression of tumor necrosis factor-activated nuclear transcription factor-kappaB, activator protein-1, c-Jun N-terminal kinase, and apoptosis by beta-lapachone. Biochem Pharmacol. 57:763-74. Marr, J.J., and R. Docampo. 1986. Chemotherapy for Chagas' disease: a perspective of current therapy and considerations for future research. Rev Infect Dis. 8:884-903. Martin, P. 1997. Wound healing--aiming for perfect skin regeneration. Science. 276:75-81. Moon, D.O., Y.H. Choi, N.D. Kim, Y.M. Park, and G.Y. Kim. 2007. Anti-inflammatory effects of beta-lapachone in lipopolysaccharide-stimulated BV2 microglia. Int Immunopharmacol. 7:506-14. Pardee, A.B., Y.Z. Li, and C.J. Li. 2002. Cancer therapy with beta-lapachone. Curr Cancer Drug Targets. 2:227-42. Parenteau, G.L., G.M. Doherty, G.R. Peplinski, K. Tsung, and J.A. Norton. 1995. Prolongation of skin allografts by recombinant tumor necrosis factor and interleukin-1. Ann Surg. 221:572-7; discussion 577-8. Pink, J.J., S. Wuerzberger-Davis, C. Tagliarino, S.M. Planchon, X. Yang, C.J. Froelich, and D.A. Boothman. 2000. Activation of a cysteine protease in MCF-7 and T47D breast cancer cells during beta-lapachone-mediated apoptosis. Exp Cell Res. 255:144-55. Pinto, A.V., M.D. Pinto, B. Gilbert, J. Pellegrino, and R.T. Mello. 1977. Schistosomiasis mansoni: blockage of cercarial skin penetration by chemical agents: i. naphthoquinones and derivatives. Trans R Soc Trop Med Hyg. 71:133-5. Planchon, S.M., J.J. Pink, C. Tagliarino, W.G. Bornmann, M.E. Varnes, and D.A. Boothman. 2001. beta-Lapachone-induced apoptosis in human prostate cancer cells: involvement of NQO1/xip3. Exp Cell Res. 267:95-106. Planchon, S.M., S. Wuerzberger, B. Frydman, D.T. Witiak, P. Hutson, D.R. Church, G. Wilding, and D.A. Boothman. 1995. Beta-lapachone-mediated apoptosis in human promyelocytic leukemia (HL-60) and human prostate cancer cells: a p53-independent response. Cancer Res. 55:3706-11. Ravelo, A.G., A. Estevez-Braun, H. Chavez-Orellana, E. Perez-Sacau, and D. Mesa-Siverio. 2004. Recent studies on natural products as anticancer agents. Curr Top Med Chem. 4:241-65. Ruszczak, Z., and R.A. Schwartz. 2000. Modern aspects of wound healing: An update. Dermatol Surg. 26:219-29. Silva, J.S., F. Ferrioli-Filho, M.M. Kanesiro, V.F. Ferreira, S.C. Santos, C.N. Pinto, J.L. Fonseca, H.E. Mizrahy, B. Gilbert, M.C. Pinto, and et al. 1992. Evaluation of some organic compounds on bloodstream forms of Trypanosoma cruzi. Mem Inst Oswaldo Cruz. 87:345-51. Singer, A.J., and R.A. Clark. 1999. Cutaneous wound healing. N Engl J Med. 341:738-46. Stadelmann, W.K., A.G. Digenis, and G.R. Tobin. 1998. Physiology and healing dynamics of chronic cutaneous wounds. Am J Surg. 176:26S-38S. Wajant, H., K. Pfizenmaier, and P. Scheurich. 2003. Tumor necrosis factor signaling. Cell Death Differ. 10:45-65. Watanabe, N., and H.J. Forman. 2003. Autoxidation of extracellular hydroquinones is a causative event for the cytotoxicity of menadione and DMNQ in A549-S cells. Arch Biochem Biophys. 411:145-57. Weller, M., S. Winter, C. Schmidt, P. Esser, A. Fontana, J. Dichgans, and P. Groscurth. 1997. Topoisomerase-I inhibitors for human malignant glioma: differential modulation of p53, p21, bax and bcl-2 expression and of CD95-mediated apoptosis by camptothecin and beta-lapachone. Int J Cancer. 73:707-14. Wood, F.M., and M. Stoner. 1996. Implication of basement membrane development on the underlying scar in partial-thickness burn injury. Burns. 22:459-62. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/42804 | - |
dc.description.abstract | β-lapachone 為一種由南美洲Lapacho tree 樹幹中萃取出來的物質,我們實驗室已證實β-lapachone 具有促進老鼠皮膚傷口癒合的能力。本實驗採用C57BL/6鼷鼠和巨噬細胞株 (RAW264.7 cells) 分別進行活體及細胞培養的研究,探討β-lapachone 對皮膚燙傷傷口癒合以及巨噬細胞增生與釋放生長因子能力的影響,實驗結果如下:(1) 動物實驗結果顯示:經內含100μM β-lapachone 的凡士林軟膏處理後,實驗組老鼠燙傷傷口 (6mm 直徑圓形,100℃,60 秒) 癒合的速度較僅敷上凡士林軟膏之控制組快。在燙傷後14 天,實驗組老鼠燙傷傷口直徑已縮為原來傷口長度的5.4%,但控制組老鼠傷口長度仍為原來的40%,具顯著差異;(2) 蘇木紫-伊紅染色和螢光免疫組織化學染色結果顯示:經100μMβ-lapachone 處理後的燙傷傷口,其組織切片的表皮層、真皮層和皮下組織都較快恢復原有的結構並出現較多的巨噬細胞;(3) 細胞培養的結果顯示:巨噬細胞在0.5μM β-lapachone 處理後24 小時,細胞增生比例為127.9%,與控制組相比,具顯著性差異,且巨噬細胞株在0.5μM β-lapachone 處理後3~24 小時,與同時間未經藥物處理的控制組相比較,細胞增生比例為105% ~ 117%;(4) 酵素免疫分析法結果顯示:先以10ng/ml TNF-α 處理5 分鐘、再加入0.5μM β-lapachone 的處理組可以使巨噬細胞在短時間內釋放最多表皮生長因子 (EGF),與控制組相比,在15 和30 分鐘時達到顯著差異;但僅加入0.5μM β-lapachone 的處理組可以使巨噬細胞釋放最多血管內皮生長因子 (VEGF)。
綜合以上結果顯示:β-lapachone 可加速燙傷傷口癒合的過程,可能的機制為透過增加巨噬細胞的增生,使其釋放較多的表皮生長因子和血管內皮生長因子,進而達到促進燙傷傷口癒合的目的。 | zh_TW |
dc.description.abstract | β-lapachone is a quinine of lapachol extracted from the bark of lapacho tree. Our recent findings demonstrated that punched skin wounds of mice healed much faster in β-lapachone treated group than in the control group (Kung et al., 2008). In this study, C57BL/6 mice were used to investigate the effects of β-lapachone on burn-wounded skin. Cell studies were done by using RAW264.7 cell line as a model for scrutinizing the effect of β-lapachone on proliferation and secretion of growth factors of macrophages. In vivo experiments revealed that wounds treated with 100μM β-lapachone recovered faster then those treated with control ointment. H&E and immunohistochemistry staining showed that wounds treated with ointment containing 100μM β-lapachone recovered faster in its epidermis, dermis, and connective tissues, and more macrophages appeared than those treated with control ointment. By MTT assay, We found that after being treated with 0.5μM β-lapachone for 24 hours, the proliferation ratio of RAW264.7 cells raised to 127.9%. The results of time course (3hr~24hr) revealed that the proliferation ratio of 0.5μM β-lapachone-treated RAW264.7 cells raised from 105%~177%, indicating that β-lapachone has reached its maximal effect within 3 hours. The effects of TNF-α and β-lapachone on the secretion of growth factors by macrophages were also analyzed by ELISA. Results indicated that the secretion of EGF by macrophages treated with “5min 10ng/ml TNF-α pretreatment + 0.5μM β-lapachone” was the highest among all five different treatments, and significance was reached at 15 and 30 minutes compared with control. In contrast, the secretion of VEGF by macrophages treated with 0.5μM β-lapachone alone was the highest.
The results obtained from the present study showed that β-lapachone might play an important role in accelerating the burned wound healing process by increasing the proliferation of macrophages and enhancing their ability to secrete EGF and VEGF. | en |
dc.description.provenance | Made available in DSpace on 2021-06-15T01:24:06Z (GMT). No. of bitstreams: 1 ntu-98-R96446008-1.pdf: 5229741 bytes, checksum: 3e1e16953436c94df1b89854d407ad4f (MD5) Previous issue date: 2009 | en |
dc.description.tableofcontents | 中文摘要 3
英文摘要 4 縮寫表 6 一、緒言 (Introduction) 7 1.1 β-lapachone 7 1.2 燙傷傷口癒合 7 1.3 生長因子:EGF、VEGF 10 1.4 腫瘤壞死因子-alpha (Tumor Necrotic Factor-alpha, TNF-α) 10 二、目的 (Purposes) 12 三、材料與方法 (Materials and Methods) 13 3.1 試劑 (Reagents) 13 3.2 活體內傷口癒合測定 (In-vivo wound-healing assay) 14 3.3 蘇木紫-伊紅染色 (H&E) 14 3.4 螢光免疫組織化學染色 (Fluorescence immunohistochemistry staining) 15 3.5 細胞培養 (Cell culture) 15 3.6 細胞存活率測定 (MTT assay) 統計分析 15 3.6.1 藥物濃度與細胞存活率測定 15 3.6.2 藥物處理時程與細胞存活率測定 16 3.7 螢光免疫細胞化學染色 (Fluorescence immunocytochemistry staining) 16 3.8 酵素免疫分析法 (Enzyme-linked immunoassay, ELISA) 16 3.9 數據統計分析 17 四、結果 (Results) 18 4.1 β-Lapachone加速實驗動物之傷口癒合 18 4.2 敷以β-Lapachone的傷口組織切片出現大量巨噬細胞 18 4.3 低濃度的β-Lapachone促進巨噬細胞增生 18 4.4 β-Lapachone於短時間內達到促使巨噬細胞增生效果 19 4.5 TNF-α與β-Lapachone共同處理可促進巨噬細胞釋放表皮生長因子 (EGF) 19 4.6 β-Lapachone可促進巨噬細胞釋放血管內皮生長因子 (VEGF) 20 五、討論 (Discussions) 22 5.1 β-Lapachone 加快實驗動物活體內傷口癒合 22 5.2 不同濃度的β-lapachone對RAW264.7細胞株會產生不同影響,在低濃度時 (<1μM) 具有增生作用,但在高濃度時 (>2.5μM) 則具有毒殺作用 23 5.3 β-lapachone會藉由促進巨噬細胞分泌EGF來加速燙傷傷口癒合 24 5.4 β-lapachone抑制巨噬細胞的發炎作用? 24 六、 結論 (Conclusions) 26 七、 未來擬繼續進行之研究工作 (Further works) 27 八、 參考文獻 (References) 28 九、 圖片說明 (Figures and Figure Legends) 31 | |
dc.language.iso | zh-TW | |
dc.title | β-Lapachone加速皮膚燙傷傷口癒合 | zh_TW |
dc.title | β-Lapachone Accelerates the Recovery of Burn-Wounded Skin | en |
dc.type | Thesis | |
dc.date.schoolyear | 97-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 錢宗良,周逸鵬 | |
dc.subject.keyword | 巨噬細胞,傷口癒合, | zh_TW |
dc.subject.keyword | β-Lapachone,EGF,VEGF, | en |
dc.relation.page | 53 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2009-07-24 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 解剖學暨生物細胞學研究所 | zh_TW |
顯示於系所單位: | 解剖學暨細胞生物學科所 |
文件中的檔案:
檔案 | 大小 | 格式 | |
---|---|---|---|
ntu-98-1.pdf 目前未授權公開取用 | 5.11 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。