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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 陳兆勛(Chau-Hsun Chen) | |
| dc.contributor.author | Ching-Feng Lin | en |
| dc.contributor.author | 林敬峰 | zh_TW |
| dc.date.accessioned | 2021-06-08T01:04:47Z | - |
| dc.date.copyright | 2014-09-05 | |
| dc.date.issued | 2014 | |
| dc.date.submitted | 2014-08-20 | |
| dc.identifier.citation | [1] International Commission on Non-Ionizing Radiation Protection. (2006). ICNIRP statement on far infrared radiation exposure. Health Physics, 91(6), 630-645.
[2] 林宜弘、廖建貴. (1996).遠紅外線輻射性能之簡單量測-逆向熱傳導法之探討，力學期刊；12(2):181-186 [3] Skoog DA, Leary JJ. Principles of Instrumental Analysis 4th Ed. Saunders College Pulishing. 1992b:254-260 [4] Skoog, D. A., & West, D. M. (1980). Principles of instrumental analysis (Vol. 158). Philadelphia: Saunders College. [5] 謝鸚爗, 林招膨, 劉威忠, & 林群智. (2007). 遠紅外線在醫學上之應用及其作用機制. 台灣應用輻射與同位素雜誌, 3(3), 333-340. [6] Lin, C. C., Chang, C. F., Lai, M. Y., Chen, T. W., Lee, P. C., & Yang, W. C. (2007). Far-infrared therapy: a novel treatment to improve access blood flow and unassisted patency of arteriovenous fistula in hemodialysis patients. Journal of the American Society of Nephrology, 18(3), 985-992. [7] Lin, C. C., Liu, X. M., Peyton, K., Wang, H., Yang, W. C., Lin, S. J., & Durante, W. (2008). Far infrared therapy inhibits vascular endothelial inflammation via the induction of heme oxygenase-1. Arteriosclerosis, thrombosis, and vascular biology, 28(4), 739-745. [8] Hwang, S., Lee, D. H., Lee, I. K., Park, Y. M., & Jo, I. (2014). Far-infrared radiation inhibits proliferation, migration, and angiogenesis of human umbilical vein endothelial cells by suppressing secretory clusterin levels. Cancer letters,346(1), 74-83. [9] Ko, W. S., Chen, T. H., Chen, C. H., Chen, T. W., & Chen, Y. C. (2012). A Non-thermal Effect of Far-infrared Activates Akt to Reduce Doxorubicin-induced Apoptosis in Human Umbilical Vein Endothelial Cells. Acta Nephrologica, 26(1), 2-7. [10] Ishibashi, J., Yamashita, K., Ishikawa, T., Hosokawa, H., Sumida, K., Nagayama, M., & Kitamura, S. (2008). The effects inhibiting the proliferation of cancer cells by far-infrared radiation (FIR) are controlled by the basal expression level of heat shock protein (HSP) 70A. Medical Oncology, 25(2), 229-237. [11] Hsu, Y. H., Chen, Y. C., Chen, T. H., Sue, Y. M., Cheng, T. H., Chen, J. R., & Chen, C. H. (2012). Far-infrared therapy induces the nuclear translocation of PLZF which inhibits VEGF-induced proliferation in human umbilical vein endothelial cells. PloS one, 7(1), e30674. [12] Udagawa, Y., Ishigame, H., & Nagasawa, H. (2002). Effects of hydroxyapatite in combination with far-infrared rays on spontaneous mammary tumorigenesis in SHN mice. The American journal of Chinese medicine, 30(04), 495-505. [13] Chang, M. H., Chen, T. H. H., Hsu, H. M., Wu, T. C., Kong, M. S., Liang, D. C., ... & Chen, D. S. (2005). Prevention of hepatocellular carcinoma by universal vaccination against hepatitis B virus: the effect and problems. Clinical cancer research, 11(21), 7953-7957. [14] Bosch, F. X., Ribes, J., & Borras, J. (1999, January). Epidemiology of primary liver cancer. In Seminars in liver disease (Vol. 19, No. 03, pp. 271-285). c 1999 by Thieme Medical Publishers, Inc.. [15] CHEN, C. J., YU, M. W., & LIAW, Y. F. (1997). Epidemiological characteristics and risk factors of hepatocellular carcinoma. Journal of gastroenterology and hepatology, 12(9‐10), S294-S308. [16] Thomas, M. B., & Zhu, A. X. (2005). Hepatocellular carcinoma: the need for progress. Journal of Clinical Oncology, 23(13), 2892-2899. [17] Takano, S., Yokosuka, O., Imazeki, F., Tagawa, M., & Omata, M. (1995). Incidence of hepatocellular carcinoma in chronic hepatitis B and C: a prospective study of 251 patients. Hepatology, 21(3), 650-655. [18] Chu, C. M. (2000). Natural history of chronic hepatitis B virus infection in adults with emphasis on the occurrence of cirrhosis and hepatocellular carcinoma.Journal of gastroenterology and hepatology, 15(s2), E25-E30. [19] Kerr, J. F., Wyllie, A. H., & Currie, A. R. (1972). Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics. British journal of cancer, 26(4), 239. [20] Kerr, J. F., Winterford, C. M., & Harmon, B. V. (1994). Apoptosis. Its significance in cancer and cancer therapy. Cancer, 73(8), 2013-2026. [21] Gerald Karp.Cell and Molecular Biology.1999:688-690 [22] G.P.Studyiaski;Cell Growth and Apoptosis.,1996. [23] Grasso, S., Menendez-Gutierrez, M. P., Carrasco-Garcia, E., Mayor-Lopez, L., Tristante, E., Rocamora-Reverte, L., ... & Martinez-Lacaci, I. (2012). Cell Death and Cancer, Novel Therapeutic Strategies. Book Section in Apoptosis and Medicine, Publisher InTech [24] Apoptosis: controlled demolition at the cellular level Rebecca C. Taylor, Sean P. Cullen & Seamus J. MartinNature Reviews Molecular Cell Biology 9, 231-241 (March 2008) [25] Zhao, Y., Li, S., Childs, E. E., Kuharsky, D. K., & Yin, X. M. (2001). Activation of pro-death Bcl-2 family proteins and mitochondria apoptosis pathway in tumor necrosis factor-α-induced liver injury. Journal of Biological Chemistry, 276(29), 27432-27440. [26] Li, S., Zhao, Y., He, X., Kim, T. H., Kuharsky, D. K., Rabinowich, H., ... & Yin, X. M. (2002). Relief of extrinsic pathway inhibition by the Bid-dependent mitochondrial release of Smac in Fas-mediated hepatocyte apoptosis. Journal of Biological Chemistry, 277(30), 26912-26920. [27] Shangary, S., & Johnson, D. E. (2002). Peptides derived from BH3 domains of Bcl-2 family members: a comparative analysis of inhibition of Bcl-2, Bcl-xL and Bax oligomerization, induction of cytochrome c release, and activation of cell death. Biochemistry, 41(30), 9485-9495. [28] Zhao, Y., Ding, W. X., Qian, T., Watkins, S., Lemasters, J. J., & Yin, X. M. (2003). Bid activates multiple mitochondrial apoptotic mechanisms in primary hepatocytes after death receptor engagement. Gastroenterology, 125(3), 854-867. [29] Li, H., Zhu, H., Xu, C. J., & Yuan, J. (1998). Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis. Cell,94(4), 491-501. [30] D’alessio, M., De Nicola, M., Coppola, S., Gualandi, G., Pugliese, L., Cerella, C., ... & Ghibelli, L. (2005). Oxidative Bax dimerization promotes its translocation to mitochondria independently of apoptosis. The FASEB journal,19(11), 1504-1506. [31] Desagher, S., Osen-Sand, A., Nichols, A., Eskes, R., Montessuit, S., Lauper, S., ... & Martinou, J. C. (1999). Bid-induced conformational change of Bax is responsible for mitochondrial cytochrome c release during apoptosis. The Journal of cell biology, 144(5), 891-901. [32] Moreau, C., Cartron, P. F., Hunt, A., Meflah, K., Green, D. R., Evan, G., ... & Juin, P. (2003). Minimal BH3 peptides promote cell death by antagonizing anti-apoptotic proteins. Journal of Biological Chemistry, 278(21), 19426-19435. [33] Gottlieb, E., Vander Heiden, M. G., & Thompson, C. B. (2000). Bcl-xL prevents the initial decrease in mitochondrial membrane potential and subsequent reactive oxygen species production during tumor necrosis factor alpha-induced apoptosis. Molecular and cellular biology, 20(15), 5680-5689. [34] Zhang, L. C., Shen, S. R., Sun, S. L., Yang, J. G., He, G. Q., & Yu, H. N. (2008). [Growth inhibition of prostate cancer cells by epigallocatechin-3-gallate in the presence of Zn2+ in vitro]. Fen zi xi bao sheng wu xue bao= Journal of molecular cell biology/Zhongguo xi bao sheng wu xue xue hui zhu ban, 41(6), 443-449. [35] Baricos, W. H., Cortez, S. L., El-Dahr, S. S., & Schnaper, H. W. (1995). ECM degradation by cultured human mesangial cells is mediated by a PA/plasmin/MMP-2 cascade. Kidney international, 47(4), 1039-1047. [36] Wang, J., & Tsirka, S. E. (2005). Neuroprotection by inhibition of matrix metalloproteinases in a mouse model of intracerebral haemorrhage. Brain,128(7), 1622-1633. [37] Kessenbrock, K., Plaks, V., & Werb, Z. (2010). Matrix metalloproteinases: regulators of the tumor microenvironment. Cell, 141(1), 52-67. [38] Bourboulia, D., & Stetler-Stevenson, W. G. (2010, June). Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs): Positive and negative regulators in tumor cell adhesion. In Seminars in cancer biology (Vol. 20, No. 3, pp. 161-168). Academic Press. [39] Llovet, J. M., Di Bisceglie, A. M., Bruix, J., Kramer, B. S., Lencioni, R., Zhu, A. X., ... & Gores, G. J. (2008). Design and endpoints of clinical trials in hepatocellular carcinoma. Journal of the National Cancer Institute, 100(10), 698-711. [40] Liabakk, N. B., Talbot, I., Smith, R. A., Wilkinson, K., & Balkwill, F. (1996). Matrix metalloprotease 2 (MMP-2) and matrix metalloprotease 9 (MMP-9) type IV collagenases in colorectal cancer. Cancer research, 56(1), 190-196. [41] Liao, H. F., Chen, Y. Y., Liu, J. J., Hsu, M. L., Shieh, H. J., Liao, H. J., ... & Chen, Y. J. (2003). Inhibitory effect of caffeic acid phenethyl ester on angiogenesis, tumor invasion, and metastasis. Journal of agricultural and food chemistry, 51(27), 7907-7912. [42] Fong, Y., Shen, K. H., Chiang, T. A., & Shih, Y. W. (2010). Acacetin Inhibits TPA‐Induced MMP‐2 and u‐PA Expressions of Human Lung Cancer Cells Through Inactivating JNK Signaling Pathway and Reducing Binding Activities of NF‐κB and AP‐1. Journal of food science, 75(1), H30-H38. [43] Liao, H. F., Chen, Y. Y., Liu, J. J., Hsu, M. L., Shieh, H. J., Liao, H. J., ... & Chen, Y. J. (2003). Inhibitory effect of caffeic acid phenethyl ester on angiogenesis, tumor invasion, and metastasis. Journal of agricultural and food chemistry, 51(27), 7907-7912. [44] Chandrashekar, N., Selvamani, A., Subramanian, R., Pandi, A., & Thiruvengadam, D. (2012). Baicalein inhibits pulmonary carcinogenesis-associated inflammation and interferes with COX-2, MMP-2 and MMP-9 expressions< i> in-vivo</i>. Toxicology and applied pharmacology, 261(1), 10-21. [45] Yu, Y. M., & Lin, H. C. (2010). Curcumin prevents human aortic smooth muscle cells migration by inhibiting of MMP-9 expression. Nutrition, Metabolism and Cardiovascular Diseases, 20(2), 125-132. [46] Chung, T. W., Moon, S. K., Chang, Y. C., Ko, J. H., Lee, Y. C., Cho, G., ... & Kim, C. H. (2004). Novel and therapeutic effect of caffeic acid and caffeic acid phenyl ester on hepatocarcinoma cells: complete regression of hepatoma growth and metastasis by dual mechanism. The FASEB Journal, 18(14), 1670-1681. [47] Lee, J. Y., Chung, T. W., Choi, H. J., Lee, C. H., Eun, J. S., Han, Y. T., ... & Ha, K. T. (2014). A novel cantharidin analog< i> N</i>-Benzylcantharidinamide reduces the expression of MMP-9 and invasive potentials of Hep3B via inhibiting cytosolic translocation of HuR. Biochemical and biophysical research communications, 447(2), 371-377. [48] Heumann, D., & Roger, T. (2002). Initial responses to endotoxins and Gram-negative bacteria. Clinica Chimica Acta, 323(1), 59-72. [49] O'Neill, G. P., & Ford-Hutchinson, A. W. (1993). Expression of mRNA for cyclooxygenase-1 and cyclooxygenase-2 in human tissues. FEBS letters,330(2), 157-160. [50] Kinoshita, T., Takahashi, Y., Sakashita, T., Inoue, H., Tanabe, T., & Yoshimoto, T. (1999). Growth stimulation and induction of epidermal growth factor receptor by overexpression of cyclooxygenases 1 and 2 in human colon carcinoma cells. Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids, 1438(1), 120-130. [51] Hu, K. Q. (2002). Rationale and feasibility of chemoprovention of hepatocellular carcinoma by cyclooxygenase-2 inhibitors. Journal of Laboratory and Clinical Medicine, 139(4), 234-243. [52] Sawaoka, H., Kawano, S., Tsuji, S., Tsujii, M., Murata, H., & Hori, M. (1998). Effects of NSAIDs on proliferation of gastric cancer cells in vitro: possible implication of cyclooxygenase-2 in cancer development. Journal of clinical gastroenterology, 27, S47-S52. [53] Bae, S. H., Jung, E. S., Park, Y. M., Kim, B. S., Kim, B. K., Kim, D. G., & Ryu, W. S. (2001). Expression of cyclooxygenase-2 (COX-2) in hepatocellular carcinoma and growth inhibition of hepatoma cell lines by a COX-2 inhibitor, NS-398. Clinical cancer research, 7(5), 1410-1418. [54] Kinoshita, T., Takahashi, Y., Sakashita, T., Inoue, H., Tanabe, T., & Yoshimoto, T. (1999). Growth stimulation and induction of epidermal growth factor receptor by overexpression of cyclooxygenases 1 and 2 in human colon carcinoma cells. Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids, 1438(1), 120-130. [55] Qiao, L., Shiff, S. J., & Rigas, B. (1998). Sulindac sulfide alters the expression of cyclin proteins in HT‐29 colon adenocarcinoma cells. International journal of cancer, 76(1), 99-104. [56] Kondo, M., Yamamoto, H., Nagano, H., Okami, J., Ito, Y., Shimizu, J., ... & Monden, M. (1999). Increased expression of COX-2 in nontumor liver tissue is associated with shorter disease-free survival in patients with hepatocellular carcinoma. Clinical cancer research, 5(12), 4005-4012. [57] G. Shiota, M. Okubo, T. Noumi, N. Noguchi, K. Oyama, K. Takano et al. (1999),Cyclooxgenase-2 expression in hepatocellular carcinoma,Hepato-gastro enterology, 46, pp. 407–412 [58] HILLEBRAND, D. J., & HASAN, M. (2003). Inhibited proliferation of cyclooxygenase-2 expressing human hepatoma cells by NS-398, a selective COX-2 inhibitor. International journal of oncology, 22, 757-763. [59] Tsujii, M., Kawano, S., Tsuji, S., Sawaoka, H., Hori, M., & DuBois, R. N. (1998). Cyclooxygenase regulates angiogenesis induced by colon cancer cells.cell, 93(5), 705-716. [60] Bae ES, Jung JW, Jang JY, Choi SK, Yoon SHC. Clinical significance of correlation between COX-2 and CD34-expression in dysplastic nodules. Hepatol- ogy. 2002;36:445A [61] Abiru, S., Nakao, K., Ichikawa, T., Migita, K., Shigeno, M., Sakamoto, M., ... & Eguchi, K. (2002). Aspirin and NS‐398 inhibit hepatocyte growth factor–induced invasiveness of human hepatoma cells. Hepatology, 35(5), 1117-1124 [62] Bae, E.S., Jung, J.W., Jang, J.Y., Choi, S.K., Yoon, S.H.C., 2002. Clinical significance of correlation between COX-2 and CD34-expression in dysplastic nodules. Hepatology, 36:445A [63] Nanji, A. A., Miao, L. I. L. I., Thomas, P. E. T. E. R., Rahemtulla, A. M. I. R., Khwaja, S. H. A. M. S. U. D. D. I. N., Zhao, S. H. U. P. I. N. G., ... & Dannenberg, A. J. (1997). Enhanced cyclooxygenase-2 gene expression in alcoholic liver disease in the rat. Gastroenterology, 112(3), 943-951. [64] Hu, K. Q., Vierling, J. M., & Redeker, A. G. (2001). Viral, host and interferon‐related factors modulating the effect of interferon therapy for hepatitis C virus infection. Journal of viral hepatitis, 8(1), 1-18. [65] Chung, C., Gottstein, J., & Blei, A. T. (2001). Indomethacin prevents the development of experimental ammonia‐induced brain edema in rats after portacaval anastomosis. Hepatology, 34(2), 249-254. [66] Kondo, M., Yamamoto, H., Nagano, H., Okami, J., Ito, Y., Shimizu, J., ... & Monden, M. (1999). Increased expression of COX-2 in nontumor liver tissue is associated with shorter disease-free survival in patients with hepatocellular carcinoma. Clinical cancer research, 5(12), 4005-4012. [67] Issaq, H. J. (2001). The role of separation science in proteomics research.Electrophoresis, 22(17), 3629. [68] 莊榮輝, Methods in Biotechnology,2nd ed,2005 [69] Elmore, S. (2007). Apoptosis: a review of programmed cell death. Toxicologic pathology, 35(4), 495-516. [70] Joza, N., Susin, S. A., Daugas, E., Stanford, W. L., Cho, S. K., Li, C. Y., ... & Penninger, J. M. (2001). Essential role of the mitochondrial apoptosis-inducing factor in programmed cell death. Nature, 410(6828), 549-554. [71] Adam-Vizi, V., & Chinopoulos, C. (2006). Bioenergetics and the formation of mitochondrial reactive oxygen species. Trends in pharmacological sciences, 27(12), 639-645. [72] Brand, M. D., Affourtit, C., Esteves, T. C., Green, K., Lambert, A. J., Miwa, S., ... & Parker, N. (2004). Mitochondrial superoxide: production, biological effects, and activation of uncoupling proteins. Free Radical Biology and Medicine, 37(6), 755-767. [73] Hoffman, D. L., Salter, J. D., & Brookes, P. S. (2007). Response of mitochondrial reactive oxygen species generation to steady-state oxygen tension: implications for hypoxic cell signaling. American Journal of Physiology-Heart and Circulatory Physiology, 292(1), H101-H108. [74] Lemasters, J. J., Nieminen, A. L., Qian, T., Trost, L. C., Elmore, S. P., Nishimura, Y., ... & Herman, B. (1998). The mitochondrial permeability transition in cell death: a common mechanism in necrosis, apoptosis and autophagy. Biochimica et Biophysica Acta (BBA)-Bioenergetics, 1366(1), 177-196. [75] Elmore, S. P., Qian, T., Grissom, S. F., & Lemasters, J. J. (2001). The mitochondrial permeability transition initiates autophagy in rat hepatocytes. The FASEB Journal, 15(12), 2286-2287. [76] Moser, C. C., Farid, T. A., Chobot, S. E., & Dutton, P. L. (2006). Electron tunneling chains of mitochondria. Biochimica et Biophysica Acta (BBA)-Bioenergetics, 1757(9), 1096-1109. [77] Wolter, K. G., Hsu, Y. T., Smith, C. L., Nechushtan, A., Xi, X. G., & Youle, R. J. (1997). Movement of Bax from the cytosol to mitochondria during apoptosis. The Journal of cell biology, 139(5), 1281-1292. [78] Gross, A., Yin, X. M., Wang, K., Wei, M. C., Jockel, J., Milliman, C., ... & Korsmeyer, S. J. (1999). Caspase cleaved BID targets mitochondria and is required for cytochrome c release, while BCL-XL prevents this release but not tumor necrosis factor-R1/Fas death. Journal of Biological Chemistry, 274(2), 1156-1163. [79] Bergers, G., Brekken, R., McMahon, G., Vu, T. H., Itoh, T., Tamaki, K., ... & Hanahan, D. (2000). Matrix metalloproteinase-9 triggers the angiogenic switch during carcinogenesis. Nature cell biology, 2(10), 737-744. [80] Stam, J. C., Michiels, F., Van der Kammen, R. A., Moolenaar, W. H., & Collard, J. G. (1998). Invasion of T‐lymphoma cells: cooperation between Rho family GTPases and lysophospholipid receptor signaling. The EMBO Journal,17(14), 4066-4074. [81] Bjorklund, M., & Koivunen, E. (2005). Gelatinase-mediated migration and invasion of cancer cells. Biochimica et Biophysica Acta (BBA)-Reviews on Cancer, 1755(1), 37-69. [82] Corry, D. B., Kiss, A., Song, L. Z., Song, L., Xu, J., Lee, S. H., ... & Kheradmand, F. (2004). Overlapping and independent contributions of MMP2 and MMP9 to lung allergic inflammatory cell egression through decreased CC chemokines. The FASEB journal, 18(9), 995-997. [83] Legrand, C., Gilles, C., Zahm, J. M., Polette, M., Buisson, A. C., Kaplan, H., ... & Tournier, J. M. (1999). Airway epithelial cell migration dynamics: MMP-9 role in cell–extracellular matrix remodeling. The Journal of cell biology, 146(2), 517-529 [84] Mohan, R., Chintala, S. K., Jung, J. C., Villar, W. V., McCabe, F., Russo, L. A., ... & Fini, M. E. (2002). Matrix metalloproteinase gelatinase B (MMP-9) coordinates and effects epithelial regeneration. Journal of Biological Chemistry,277(3), 2065-2072. [85] Reuter, B. K., Asfaha, S., Buret, A., Sharkey, K. A., & Wallace, J. L. (1996). Exacerbation of inflammation-associated colonic injury in rat through inhibition of cyclooxygenase-2. Journal of Clinical Investigation, 98(9), 2076. [86] Tsujii, M., Kawano, S., Tsuji, S., Sawaoka, H., Hori, M., & DuBois, R. N. (1998). Cyclooxygenase regulates angiogenesis induced by colon cancer cells.cell, 93(5), 705-716. [87] Sawaoka, H., Tsuji, S., Tsujii, M., Gunawan, E. S., Sasaki, Y., Kawano, S., & Hori, M. (1999). Cyclooxygenase inhibitors suppress angiogenesis and reduce tumor growth in vivo. Laboratory investigation; a journal of technical methods and pathology, 79(12), 1469-1477. [88] Tsujii, M., Kawano, S., & DuBois, R. N. (1997). Cyclooxygenase-2 expression in human colon cancer cells increases metastatic potential. Proceedings of the National Academy of Sciences, 94(7), 3336-3340. [89] HILLEBRAND, D. J., & HASAN, M. (2003). Inhibited proliferation of cyclooxygenase-2 expressing human hepatoma cells by NS-398, a selective COX-2 inhibitor. International journal of oncology, 22, 757-763. [90] Kern, M. A., Schubert, D., Sahi, D., Schoneweis, M. M., Moll, I., Haugg, A. M., ... & Schirmacher, P. (2002). Proapoptotic and antiproliferative potential of selective cyclooxygenase‐2 inhibitors in human liver tumor cells. Hepatology,36(4), 885-894. [91] Cheng, A. S., Chan, H. L., Leung, W. K., Wong, N., Johnson, P. J., & Sung, J. J. (2003). Specific COX-2 inhibitor, NS-398, suppresses cellular proliferation and induces apoptosis in human hepatocellular carcinoma cells. International journal of oncology, 23(1), 113-120. [92] Tsujii, M., Kawano, S., & DuBois, R. N. (1997). Cyclooxygenase-2 expression in human colon cancer cells increases metastatic potential. Proceedings of the National Academy of Sciences, 94(7), 3336-3340. [93] Saja K., Babu M. S. and Karunagaran D. (2007), “Anti-inflammatory Effect of Curcumin Involves Downregulation of MMP-9 in Bloo Mononuclcells,” [94] Apoptosis: controlled demolition at the cellular level Rebecca C. Taylor, Sean P. Cullen & Seamus J. MartinNature Reviews Molecular Cell Biology 9, 231-241 (March 2008) [95] Lin, C. C., Chung, M. Y., Yang, W. C., Lin, S. J., & Lee, P. C. (2013). Length polymorphisms of heme oxygenase-1 determine the effect of far-infrared therapy on the function of arteriovenous fistula in hemodialysis patients: a novel physicogenomic study. Nephrology Dialysis Transplantation, 28(5), 1284-1293. [96] Honda K, Inoue S. Sleep-enhancing effects of ar-infrared radiation in rats. Int J Biometeorol 1988;32:92-94 | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/18429 | - |
| dc.description.abstract | 肝癌是全世界最普遍的癌症之一，在台灣也常常冠居全台年癌症致死率最高之首。在眾多治療癌症的方法中，仍是以抗癌藥物的開發為最有效的治療方法。至今仍然沒有一個有效的非藥物性治療方法。是故尋找一個非藥物性的治療是我們的目的。遠紅外線為一波長介於4~1000微米之不可見光，其照射人體後所產生之熱效應與非熱效應在醫學物理治療上已被廣泛的討論。非熱效應在中醫的理論中被視為氣，也就是能量的表現。近年來遠紅外線也在西方醫療中逐漸被重視，除了已經被證實在人體內膜的發炎表現途徑中能夠透過誘導血紅素加氧酶-1（HO-1）表現進而抑制血管發炎，亦在口腔癌跟齒齦癌的研究上證實經由遠紅外線之非熱效應照射後其癌細胞的增生明顯被抑制。本實驗之目的是希望藉由Morphology assay、Migration assay、Wound healing assay、Western blot、Zymography了解肝癌細胞在受到遠紅外線照射後之細胞凋亡、轉移、增生的變化，並且探討非熱效應。由Morphology assay了解到細胞萎縮、凋亡的現象，並且由Migration assay 與Wound healing assay了解到細胞轉移、爬行的能力與增生能力的下降。由Bax蛋白的上調與Bcl-2蛋白的下調我們了解FIR或許能夠透過粒線體凋亡的途徑誘導Hep3B凋亡，並由Caspase3蛋白的表現應證凋亡途徑的產生。環氧合酶-2（Cyclooxygenase-2；COX-2）與基質金屬蛋白酶(Matrix metallo proteinases；MMPs)是癌症轉移及發炎反應、血管增生、細胞增生過程中主要參與的蛋白。在現行的抗癌藥物開發中COX-2抑制劑與MMP-9抑制劑已是治療癌症的標把藥物。透過Western blot我們發現癌細胞Hep3B在經過遠紅外線照射後其COX-2蛋白與MMP9蛋白的活性明顯的被抑制，且證實非熱效應參與了其中之調控。這樣的結果是遠紅外線能夠抑制癌細胞的生長強而有力的證據。未來是否能夠做為一個抑制肝癌的物理性治療，進一步做活體動物實驗與配合藥物做複合式的實驗使治療達到效率最佳化化，都是未來可以研究的方向。 | zh_TW |
| dc.description.abstract | Human Hepatocellular carcinoma(HHC) is one of the most common cancers in the world, it always got the highest fatality rate than any other cancers for decades in Taiwan. To increase the survival rate or reduce the fatality rate, it is necessary and important to find a way to do that, the invention of anti-cancer drugs is still considered a main way to heal HHC, there isn’t a physical treatment to be proved that can heal HHC in the world. Therefore, finding a sufficient physical way is our propose. The Far-infrared radiation(FIR) is used to being a physical treatment in Traditional Chinese Medicine(TCM) for a long time. It is getting attention Western Medicine in recent years. Not only is FIR being proved that can reduce angiogenesis in human body but also it can reduce the proliferation in tongue cancer and lung cancer by reducing HSP70 expression level. Our experiment is to show the effect of FIR in HHC. By Morphology assay、Migration assay、Wound healing assay ,we know that FIR can cause HHC to death and reduce the level of migration and proliferation. By overexpression level of Bax and inhibit expression level of Bcl-2,we know that FIR cause the crash of mitochondrial outer membrane permeabilization (MOMP) balance and induce apoptosis, and by the expression of Caspase 3 we can prove that apoptosis happened. By reducing the expression of COX-2 and MMP9, the outcome shows that FIR can inhibit migration of Hep3B,and also it can inhibit angiogenesis and proliferation. This is a sufficient evidence that FIR can reduce Hep3B in many ways. The effect of experiment FIR in mice or experiment FIR with anti-drugs can be foreseen for the Hep3B. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-08T01:04:47Z (GMT). No. of bitstreams: 1 ntu-103-R01543064-1.pdf: 2663394 bytes, checksum: 8a090f3f9da1b0d5048c5532d423d620 (MD5) Previous issue date: 2014 | en |
| dc.description.tableofcontents | 口試委員會審定書 #
誌謝 1 中文摘要 2 ABSTRACT 3 CONTENTS 4 Chapter 1 諸論 8 1.1 研究背景 8 1.1.1 遠紅外線 8 1. 從中醫角度看遠紅外線 9 2. 由西醫的角度看遠紅外線 10 3. FTIR簡介 11 1.1.2 肝癌簡介 11 1.1.3 細胞凋亡(Apoptosis) 12 1. 形態特徵 12 2. 訊號傳導路徑 13 3. 參與凋亡相關蛋白 16 1.2 研究目標: 21 探討遠紅外線(FIR)對肝癌細胞株Hep3B之Morphology分析 21 探討遠紅外線(FIR)對肝癌細胞株Hep3B之wounding healing分析 21 探討遠紅外線(FIR) 肝癌細胞株Hep3B之Migration分析 21 探討遠紅外線(FIR) 肝癌細胞株Hep3B之凋亡路徑 21 Chapter 2 實驗材料與方法 22 2.1 遠紅外線儀器 22 2.2 細胞培養 22 2.3 Morphology assay 24 2.4 Migration Assey(Boyden Chamber Assay) 25 2.5 Wound healing assay 25 2.6 Western blot 26 2.6.1 蛋白質定量 26 2.6.2 聚丙烯醯胺膠體電泳&抗體接合 28 2.7 明膠基質金屬蛋白酵素活性測試 34 Chapter 3 實驗結果 36 3.1 Morphology assay 36 3.2 Migration assay 36 3.3 Wound healing assay 37 3.4 Western blot 38 3.5 明膠基質金屬蛋白酵素活性測試 39 Chapter 4 討論 40 4.1 FIR照射後可使肝癌細胞粒線體內外膜通透性改變並誘導凋亡 40 4.2 FIR照射可使肝癌細胞MMPs之下調 42 4.3 FIR照射可使肝癌細胞之COX-2下調 44 4.4 FIR照射與熱處理做比較 46 Chapter 5 結論 49 Chapter 6 實驗數據 51 6.1 Morphology assay 51 6.2 Migration assay 53 6.3 Wound healing assay 54 6.4 Western blot 56 附錄 66 REFERENCE 70 LIST OF FIGURES Fig. 1.1細胞凋亡的型態特徵 13 Fig. 1.2 Intrinsic & Extrinsic pathway 16 Fig. 1.3 Caspase classification and activation 17 Fig. 2.1 遠紅外線岩盤床光學頻譜圖 22 Fig. 2.2 Coomassie Brilliant Blue G-250 測量蛋白濃度 27 Fig. 2.3 蛋白質電荷改變與環境PH值影響 29 Fig. 2.4 SDS蛋白變性處理 29 Fig. 2.5 Sample:SDS蛋白 30 Fig. 2.6 電泳通電內部示意圖 30 Fig. 2.7 轉印及免疫染色流程 31 Fig. 2.8 抗體抓取原理 31 Fig. 4.1FIR誘導之粒線體凋亡途徑 41 Fig. 4.2經FIR照射後MMP9蛋白誘導之途徑 44 Fig. 4.3經FIR照射後COX-2誘導之途徑 46 Fig. 5.1.1經由FIR照射後Hep3B被抑制能力圖……………………………………45 Fig. 6.1(A) Morphology assay 51 Fig. 6.1(B) Hep3B Morphology Rate……………………………………..……………47 Fig. 6.2(A)Migration assay 48 Fig. 6.2(B) Hep3B Cell Migration Number………………….………………………...48 Fig. 6.3(A) Hep3B受到遠紅外線照射60min後與Control組之比較圖 49 Fig. 6.3(B)Hep3B受到遠紅外線照射120min後與Control組之比較圖……………49 Fig. 6.3(C)定量Wound healing assay……………………………………………….....50 Fig. 6.4(A)Western blot Bax&Bcl-2 56 Fig. 6.4(B) Bax Optical dencity 56 Fig. 6.4(C) Bcl-2 Optical dencity 57 Fig. 6.4(D)定量Western Bax/Bcl-2比值………………………………...............57 Fig.6.4(E) Western blot Caspase3 58 Fig. 6.4(F) Caspase3 Optical dencity 58 Fig. 6.4(G) Western blot COX-2&MMP9 59 Fig. 6.4(H) COX-2 Optical dencity 59 Fig. 6.4(I) MMP9 Optical dencity 59 Fig. 6.4(J)Western blot Bax&Bcl-2 FIR&Heat 60 Fig. 6.4(K) Bax Optical dencity FIR&Heat 60 Fig. 6.4(L) Bcl-2 Optical dencity FIR&Heat 61 Fig. 6.4(M)定量Western Bax/Bcl-2比值 FIR&Heat………………………...............61 Fig.6.4(N) Western blot Caspase3 FIR&Heat 62 Fig. 6.4(O) Caspase3 Optical dencity FIR&Heat 62 Fig. 6.4(P) Western blot COX-2&MMP9 FIR&Heat 62 Fig. 6.4(Q) COX-2 Optical dencity FIR&Heat 63 Fig. 6.4(R) MMP9 Optical dencity FIR&Heat 63 Fig. 6.4(S) Zymography分析MMP-9蛋白活性表現量FIR&Heat 64 Fig. 6.4(T)Bax/Bcl、Caspase3、MMP-9、COX-2蛋白之FIR與Heat表現量差異.65 | |
| dc.language.iso | zh-TW | |
| dc.title | 遠紅外線對肝癌的影響 | zh_TW |
| dc.title | The effect of Far-infrared radiation (FIR)
in Human Hepatocellular carcinoma | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 102-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 楊智偉(Chih-Wei Yang),趙效明(Chao-Ming Zhao) | |
| dc.subject.keyword | 肝癌,Hep3B,FIR,細胞凋亡,轉移,Caspase3,Bax,Bcl-2,MMP9,COX-2,非熱效應, | zh_TW |
| dc.subject.keyword | HHC,Hep3B,FIR,Apoptosis,Migration,Bax,Bcl-2,Caspase3,MMP9,COX-2, | en |
| dc.relation.page | 82 | |
| dc.rights.note | 未授權 | |
| dc.date.accepted | 2014-08-20 | |
| dc.contributor.author-college | 工學院 | zh_TW |
| dc.contributor.author-dept | 應用力學研究所 | zh_TW |
| 顯示於系所單位： | 應用力學研究所 | |
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