請用此 Handle URI 來引用此文件:
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/93626完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 廖憶純 | zh_TW |
| dc.contributor.advisor | Yi-Chun Liao | en |
| dc.contributor.author | 彭齡葶 | zh_TW |
| dc.contributor.author | Ling-Ting Peng | en |
| dc.date.accessioned | 2024-08-06T16:23:04Z | - |
| dc.date.available | 2024-08-08 | - |
| dc.date.copyright | 2024-08-06 | - |
| dc.date.issued | 2024 | - |
| dc.date.submitted | 2024-07-26 | - |
| dc.identifier.citation | 1. Mueller, K., Inflammation. inflammation's yin-yang. introduction. Science, 2013. 339(6116): p. 155.
2. Wang, S., et al., Luteolin alters macrophage polarization to inhibit inflammation. Inflammation, 2020. 43(1): p. 95-108. 3. Sherwood, E.R. and T. Toliver-Kinsky, Mechanisms of the inflammatory response. Best Pract Res Clin Anaesthesiol, 2004. 18(3): p. 385-405. 4. Barton, G.M., A calculated response: control of inflammation by the innate immune system. The Journal of Clinical Investigation, 2008. 118(2): p. 413-420. 5. Bianchi, M.E., DAMPs, PAMPs and alarmins: all we need to know about danger. J Leukoc Biol, 2007. 81(1): p. 1-5. 6. Herrero-Fernandez, B., et al., Immunobiology of atherosclerosis: a complex net of interactions. Int J Mol Sci, 2019. 20(21). 7. Chen, L., et al., Inflammatory responses and inflammation-associated diseases in organs. Oncotarget, 2018. 9(6): p. 7204-7218. 8. Chen, S., et al., Epigenetic regulation of macrophages: from homeostasis maintenance to host defense. Cell Mol Immunol, 2020. 17(1): p. 36-49. 9. Shapouri-Moghaddam, A., et al., Macrophage plasticity, polarization, and function in health and disease. J Cell Physiol, 2018. 233(9): p. 6425-6440. 10. Rőszer, T., Understanding the mysterious M2 macrophage through activation markers and effector mechanisms. Mediators Inflamm, 2015. 2015: p. 816460. 11. Wang, N., H. Liang, and K. Zen, Molecular mechanisms that influence the macrophage m1-m2 polarization balance. Front Immunol, 2014. 5: p. 614. 12. Ananthakrishnan, A.N., Epidemiology and risk factors for IBD. Nat Rev Gastroenterol Hepatol, 2015. 12(4): p. 205-17. 13. Saez, A., et al., Pathophysiology of inflammatory bowel disease: innate immune system. Int J Mol Sci, 2023. 24(2). 14. Seyedian, S.S., F. Nokhostin, and M.D. Malamir, A review of the diagnosis, prevention, and treatment methods of inflammatory bowel disease. J Med Life, 2019. 12(2): p. 113-122. 15. Zhang, Y.Z. and Y.Y. Li, Inflammatory bowel disease: pathogenesis. World J Gastroenterol, 2014. 20(1): p. 91-9. 16. Guan, Q., A comprehensive review and update on the pathogenesis of inflammatory bowel disease. Journal of Immunology Research, 2019. 2019: p. 7247238. 17. Baumgart, D.C. and W.J. Sandborn, Inflammatory bowel disease: clinical aspects and established and evolving therapies. Lancet, 2007. 369(9573): p. 1641-57. 18. Yamamoto, S. and X. Ma, Role of Nod2 in the development of Crohn's disease. Microbes Infect, 2009. 11(12): p. 912-8. 19. Abraham, C. and J.H. Cho, Inflammatory bowel disease. N Engl J Med, 2009. 361(21): p. 2066-78. 20. Cobrin, G.M. and M.T. Abreu, Defects in mucosal immunity leading to Crohn's disease. Immunol Rev, 2005. 206: p. 277-95. 21. Flynn, S. and S. Eisenstein, Inflammatory bowel disease presentation and diagnosis. Surg Clin North Am, 2019. 99(6): p. 1051-1062. 22. Ordás, I., et al., Ulcerative colitis. Lancet, 2012. 380(9853): p. 1606-19. 23. Khor, B., A. Gardet, and R.J. Xavier, Genetics and pathogenesis of inflammatory bowel disease. Nature, 2011. 474(7351): p. 307-17. 24. Sheng, Q., et al., Ursolic acid regulates intestinal microbiota and inflammatory cell infiltration to prevent ulcerative colitis. J Immunol Res, 2021. 2021: p. 6679316. 25. Furrie, E., et al., Systemic antibodies towards mucosal bacteria in ulcerative colitis and Crohn's disease differentially activate the innate immune response. Gut, 2004. 53(1): p. 91-8. 26. Farrell, R.J. and M.A. Peppercorn, Ulcerative colitis. Lancet, 2002. 359(9303): p. 331-40. 27. Segal, J.P., J.F. LeBlanc, and A.L. Hart, Ulcerative colitis: an update. Clin Med (Lond), 2021. 21(2): p. 135-139. 28. Du, L. and C. Ha, Epidemiology and pathogenesis of ulcerative colitis. Gastroenterol Clin North Am, 2020. 49(4): p. 643-654. 29. Kaenkumchorn, T. and G. Wahbeh, Ulcerative colitis: making the diagnosis. Gastroenterol Clin North Am, 2020. 49(4): p. 655-669. 30. Perrin, A., Anatomy and physiology of the gastrointestinal tract and associated disease processes, in Stoma Care Specialist Nursing: A Guide for Clinical Practice, M. White and A. Perrin, Editors. 2023, Springer International Publishing: Cham. p. 39-54. 31. Ogobuiro, I., et al., Physiology, gastrointestinal, in StatPearls. 2023: Treasure Island (FL). 32. Gustafsson, J.K. and M.E.V. Johansson, The role of goblet cells and mucus in intestinal homeostasis. Nat Rev Gastroenterol Hepatol, 2022. 19(12): p. 785-803. 33. Xiong, T., et al., Ganluyin ameliorates DSS-induced ulcerative colitis by inhibiting the enteric-origin LPS/TLR4/NF-κB pathway. J Ethnopharmacol, 2022. 289: p. 115001. 34. Gadaleta, R.M., et al., Farnesoid X receptor activation inhibits inflammation and preserves the intestinal barrier in inflammatory bowel disease. Gut, 2011. 60(4): p. 463-72. 35. Li, H., et al., Protective role of berberine on ulcerative colitis through modulating enteric glial cells-intestinal epithelial cells-immune cells interactions. Acta Pharm Sin B, 2020. 10(3): p. 447-461. 36. Parikh, K., et al., Colonic epithelial cell diversity in health and inflammatory bowel disease. Nature, 2019. 567(7746): p. 49-55. 37. Cai, Z., S. Wang, and J. Li, Treatment of inflammatory bowel disease: a comprehensive review. Front Med (Lausanne), 2021. 8: p. 765474. 38. Korzenik, J.R. and D.K. Podolsky, Evolving knowledge and therapy of inflammatory bowel disease. Nat Rev Drug Discov, 2006. 5(3): p. 197-209. 39. Wright, E.K., N.S. Ding, and O. Niewiadomski, Management of inflammatory bowel disease. Med J Aust, 2018. 209(7): p. 318-323. 40. Yao, S., et al., Bifidobacterium longum: protection against inflammatory bowel disease. J Immunol Res, 2021. 2021: p. 8030297. 41. Higashiyama, M. and R. Hokaria, New and emerging treatments for inflammatory bowel disease. Digestion, 2023. 104(1): p. 74-81. 42. Chang, Q., et al., Physicochemical properties and antioxidant capacity of chinese olive (Canarium album L.) cultivars. J Food Sci, 2017. 82(6): p. 1369-1377. 43. Kuo, C.T., et al., Antioxidant and antiglycation properties of different solvent extracts from Chinese olive (Canarium album L.) fruit. Asian Pac J Trop Med, 2015. 8(12): p. 1013-1021. 44. Hsieh, S.C., et al., The methanol-ethyl acetate partitioned fraction from Chinese olive fruits inhibits cancer cell proliferation and tumor growth by promoting apoptosis through the suppression of the NF-κB signaling pathway. Food Funct, 2016. 7(12): p. 4797-4803. 45. Yeh, Y.T., A.N. Chiang, and S.C. Hsieh, Chinese olive (Canarium album L.) fruit extract attenuates metabolic dysfunction in diabetic rats. Nutrients, 2017. 9(10). 46. Yeh, Y.T., et al., Chinese olive extract ameliorates hepatic lipid accumulation in vitro and in vivo by regulating lipid metabolism. Sci Rep, 2018. 8(1): p. 1057. 47. Yeh, Y.T., et al., Chinese olive (Canarium album L.) fruit regulates glucose utilization by activating AMP-activated protein kinase. Faseb j, 2020. 34(6): p. 7866-7884. 48. Li, I.-S., Effects of Chinese olive (Canarium album L.) fruit extract on attenuating TNBS-induced colitis in mice. 2021. 49. Lim, W.-K., Effects of Chinese olive (Canarium album L.) fruit extract on attenuating DSS-induced ulceative colitis in mice. 2023. 50. Kuo, Y.H., et al., Identification and structural elucidation of anti-inflammatory compounds from Chinese olive (Canarium Album L.) fruit extracts. Foods, 2019. 8(10). 51. Đorović, J., et al., Influence of different free radicals on scavenging potency of gallic acid. J Mol Model, 2014. 20(7): p. 2345. 52. Sohrabi, F., et al., Gallic acid suppresses inflammation and oxidative stress through modulating Nrf2-HO-1-NF-κB signaling pathways in elastase-induced emphysema in rats. Environ Sci Pollut Res Int, 2021. 28(40): p. 56822-56834. 53. Jiang, Y., et al., Gallic acid: a potential anti-cancer agent. Chin J Integr Med, 2022. 28(7): p. 661-671. 54. Bai, J., et al., Gallic acid: pharmacological activities and molecular mechanisms involved in inflammation-related diseases. Biomed Pharmacother, 2021. 133: p. 110985. 55. Seo, C.S., et al., Quantitative analysis and In vitro anti-inflammatory effects of gallic acid, ellagic acid, and quercetin from radix sanguisorbae. Pharmacogn Mag, 2016. 12(46): p. 104-8. 56. Girish, C. and S.C. Pradhan, Drug development for liver diseases: focus on picroliv, ellagic acid and curcumin. Fundam Clin Pharmacol, 2008. 22(6): p. 623-32. 57. Zeb, A., Ellagic acid in suppressing in vivo and in vitro oxidative stresses. Mol Cell Biochem, 2018. 448(1-2): p. 27-41. 58. Rogerio, A.P., et al., Anti-inflammatory effects of Lafoensia pacari and ellagic acid in a murine model of asthma. Eur J Pharmacol, 2008. 580(1-2): p. 262-70. 59. Mohammadinejad, A., et al., Ellagic acid as a potent anticancer drug: a comprehensive review on in vitro, in vivo, in silico, and drug delivery studies. Biotechnol Appl Biochem, 2022. 69(6): p. 2323-2356. 60. Zhu, H., et al., Ellagic acid and its anti-aging effects on central nervous system. Int J Mol Sci, 2022. 23(18). 61. Gupta, A., et al., Neuroprotective potential of ellagic acid: a critical review. Adv Nutr, 2021. 12(4): p. 1211-1238. 62. Saeidnia, S., et al., The story of beta-sitosterol- a Review. European Journal of Medicinal Plants, 2014. 4(5): p. 590-609. 63. GHOSAL, S. and K. Saini, Sitoindosides I and II, two new anti-ulcerogenic sterylacylglucodises from Musa paradisiaca. Journal of chemical research. Synopses (Print), 1984(4). 64. Bouic, P.J., et al., Beta-sitosterol and beta-sitosterol glucoside stimulate human peripheral blood lymphocyte proliferation: implications for their use as an immunomodulatory vitamin combination. Int J Immunopharmacol, 1996. 18(12): p. 693-700. 65. Lee, J.H., et al., Immunoregulatory activity by daucosterol, a beta-sitosterol glycoside, induces protective Th1 immune response against disseminated candidiasis in mice. Vaccine, 2007. 25(19): p. 3834-40. 66. Hernández-Valle, E., et al., Anti-inflammatory effect of 3-O-[(6'-O-palmitoyl)-β-D-glucopyranosyl sitosterol] from agave angustifolia on ear edema in mice. Molecules, 2014. 19(10): p. 15624-37. 67. Qiu, S., et al., Amentoflavone inhibits tumor necrosis factor-α-induced migration and invasion through AKT/mTOR/S6k1/hedgehog signaling in human breast cancer. Food Funct, 2021. 12(20): p. 10196-10209. 68. Chen, W.T., et al., Amentoflavone induces cell-cycle arrest, apoptosis, and invasion inhibition in non-small cell lung cancer cells. Anticancer Res, 2021. 41(3): p. 1357-1364. 69. An, J., et al., Amentoflavone protects against psoriasis-like skin lesion through suppression of NF-κB-mediated inflammation and keratinocyte proliferation. Mol Cell Biochem, 2016. 413(1-2): p. 87-95. 70. Cai, J., et al., Amentoflavone ameliorates cold stress-induced inflammation in lung by suppression of C3/BCR/NF-κB pathways. BMC Immunol, 2019. 20(1): p. 49. 71. Wang, H.Y., et al., Protocatechuic acid inhibits inflammatory responses in LPS-stimulated BV2 microglia via NF-κB and MAPKs signaling pathways. Neurochem Res, 2015. 40(8): p. 1655-60. 72. Wongwichai, T., et al., Anthocyanins and metabolites from purple rice inhibit IL-1β-induced matrix metalloproteinases expression in human articular chondrocytes through the NF-κB and ERK/MAPK pathway. Biomed Pharmacother, 2019. 112: p. 108610. 73. Nam, Y.J. and C.S. Lee, Protocatechuic acid inhibits Toll-like receptor-4-dependent activation of NF-κB by suppressing activation of the Akt, mTOR, JNK and p38-MAPK. Int Immunopharmacol, 2018. 55: p. 272-281. 74. Chao, C.Y. and M.C. Yin, Antibacterial effects of roselle calyx extracts and protocatechuic acid in ground beef and apple juice. Foodborne Pathog Dis, 2009. 6(2): p. 201-6. 75. Wang, Q., et al., Protocatechuic acid protects mice from influenza A virus infection. Eur J Clin Microbiol Infect Dis, 2022. 41(4): p. 589-596. 76. Shi, G.F., et al., Alpinia protocatechuic acid protects against oxidative damage in vitro and reduces oxidative stress in vivo. Neurosci Lett, 2006. 403(3): p. 206-10. 77. Pandurangan, A.K., et al., Gallic acid suppresses inflammation in dextran sodium sulfate-induced colitis in mice: possible mechanisms. Int Immunopharmacol, 2015. 28(2): p. 1034-43. 78. Yu, T.Y., et al., Gallic acid ameliorates dextran sulfate sodium-induced ulcerative colitis in mice via inhibiting NLRP3 inflammasome. Front Pharmacol, 2023. 14: p. 1095721. 79. Jin, H., et al., Ellagic acid prevents gut damage via ameliorating microbe-associated intestinal lymphocyte imbalance. Food Funct, 2022. 13(19): p. 9822-9831. 80. Kim, D.H., et al., Ellagic acid prevented dextran-sodium-sulfate-induced colitis, liver, and brain injury through gut microbiome changes. Antioxidants (Basel), 2023. 12(10). 81. Sakthivel, K.M. and C. Guruvayoorappan, Amentoflavone inhibits iNOS, COX-2 expression and modulates cytokine profile, NF-κB signal transduction pathways in rats with ulcerative colitis. Int Immunopharmacol, 2013. 17(3): p. 907-16. 82. Farombi, E.O., et al., Dietary protocatechuic acid ameliorates dextran sulphate sodium-induced ulcerative colitis and hepatotoxicity in rats. Food Funct, 2016. 7(2): p. 913-21. 83. So, B.R., et al., Dietary protocatechuic acid redistributes tight junction proteins by targeting Rho-associated protein kinase to improve intestinal barrier function. Food Funct, 2023. 14(10): p. 4777-4791. 84. Yang, X., et al., Protocatechuic acid alleviates dextran-sulfate-sodium-induced ulcerative colitis in mice via the regulation of intestinal flora and ferroptosis. Molecules, 2023. 28(9). 85. Zhu, Y., M. Zhu, and P. Lance, iNOS signaling interacts with COX-2 pathway in colonic fibroblasts. Exp Cell Res, 2012. 318(16): p. 2116-27. 86. You, Y., et al., Postbiotic muramyl dipeptide alleviates colitis via activating autophagy in intestinal epithelial cells. Front Pharmacol, 2022. 13: p. 1052644. 87. Zeng, W., et al., Elevated ZIPK is required for TNF-α-induced cell adhesion molecule expression and leucocyte adhesion in endothelial cells. Acta Biochim Biophys Sin (Shanghai), 2021. 53(5): p. 567-574. 88. Yunna, C., et al., Macrophage M1/M2 polarization. Eur J Pharmacol, 2020. 877: p. 173090. 89. Wang, F., et al., Interferon gamma induces reversible metabolic reprogramming of M1 macrophages to sustain cell viability and pro-inflammatory activity. EBioMedicine, 2018. 30: p. 303-316. 90. Bain, C.C. and A. Schridde, Origin, differentiation, and function of intestinal macrophages. Front Immunol, 2018. 9: p. 2733. 91. Agoro, R., et al., Cell iron status influences macrophage polarization. PLoS One, 2018. 13(5): p. e0196921. 92. Zhu, W., et al., Disequilibrium of M1 and M2 macrophages correlates with the development of experimental inflammatory bowel diseases. Immunol Invest, 2014. 43(7): p. 638-52. 93. Waqas, S.F.H., G. Ampem, and T. Röszer, Analysis of IL-4/STAT6 signaling in macrophages. Methods Mol Biol, 2019. 1966: p. 211-224. 94. Thuy, P.T. and N.T. Son, Thermodynamic and kinetic studies on antioxidant capacity of amentoflavone: a DFT (density functional theory) computational approach. Free Radic Res, 2022. 56(7-8): p. 526-535. 95. Al Olayan, E.M., et al., Protocatechuic acid mitigates cadmium-induced neurotoxicity in rats: Role of oxidative stress, inflammation and apoptosis. Sci Total Environ, 2020. 723: p. 137969. 96. Pérez, S. and S. Rius-Pérez, Macrophage polarization and reprogramming in acute inflammation: a redox perspective. Antioxidants (Basel), 2022. 11(7). 97. Lissner, D., et al., Monocyte and M1 macrophage-induced barrier defect contributes to chronic intestinal inflammation in IBD. Inflamm Bowel Dis, 2015. 21(6): p. 1297-305. 98. Lu, Y., et al., Total polysaccharides of the Sijunzi decoction attenuate tumor necrosis factor-α-induced damage to the barrier function of a Caco-2 cell monolayer via the nuclear factor-κB-myosin light chain kinase-myosin light chain pathway. World J Gastroenterol, 2018. 24(26): p. 2867-2877. 99. Fasano, A., Intestinal permeability and its regulation by zonulin: diagnostic and therapeutic implications. Clin Gastroenterol Hepatol, 2012. 10(10): p. 1096-100. 100. Escudero-Hernández, C. and S. Koch, The epithelial barrier, in Molecular Genetics of Inflammatory Bowel Disease, C. Hedin, J.D. Rioux, and M. D'Amato, Editors. 2019, Springer International Publishing: Cham. p. 329-345. | - |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/93626 | - |
| dc.description.abstract | 腸道發炎與發炎性腸道疾病 (inflammatory bowel disease, IBD) 密切相關。IBD 是一種腸道慢性、反覆性持續發炎的疾病,會導致腸道組織的損傷、潰瘍、纖維化以及腸道屏障功能的破壞。我們的研究旨在探索治療 IBD 的天然化合物,我們已經證實中國橄欖 (Canarium album L.) 的果實萃取物 (簡稱 COE) 具有抗發炎功效,可抑制促發炎細胞因子、inducible nitric oxide synthase (iNOS) 和 cyclooxygenase-2 (COX-2) 的表達。COE 也能改善 IBD 的發炎狀況,減輕潰瘍性結腸炎 (ulcerative colitis, UC) 小鼠腸道上皮的損傷和免疫細胞的浸潤,並降低結腸組織中細胞黏附蛋白質 intercellular adhesion molecule-1 (ICAM-1) 和 selectin-E 的表達。謝淑貞教授的實驗室鑑定出 COE 中具有抗發炎作用的生物活性化合物,包括沒食子酸 (gallic acid, GA)、鞣花酸 (ellagic acid, EA)、sitoindoside I (SI)、amentoflavone (AMF) 和原兒茶酸 (protocatechuic acid, PA)。本研究進一步探討這五種化合物對腸道屏障功能及免疫反應的調節作用。結果顯示,這五種化合物能降低脂多醣 (lipopolysaccharide, LPS) 誘導的 RAW264.7 小鼠巨噬細胞中之COX-2 和 iNOS 的蛋白質含量,減少促發炎型的 M1 巨噬細胞並增加抗發炎型的 M2 巨噬細胞,還會改善發炎的腸道上皮細胞 CCD841的屏障功能,和降低單核細胞 THP-1 對 CCD841 細胞的附著。總結來說,我們的研究突顯出 COE中生物活性成分的抗發炎潛力,在保護腸道健康方面具有重要意義,並為進一步研究這些化合物的作用機制及其在臨床的應用開啟了新的方向。 | zh_TW |
| dc.description.abstract | Intestinal inflammation is closely associated with inflammatory bowel disease (IBD), a chronic, recurrent condition causing persistent intestinal inflammation, tissue damage, ulceration, fibrosis, and disrupted barrier function. Our research aims to explore natural compounds for the treatment of IBD. We have demonstrated that Chinese olive (Canarium album L.) fruit extract, known as COE, has anti-inflammatory properties. COE inhibits the expression of pro-inflammatory cytokines, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). COE also alleviates inflammation in IBD by reducing epithelial damage and immune cell infiltration in a mouse model of ulcerative colitis (UC), and decreasing intercellular adhesion molecule-1 (ICAM-1) and selectin-E expression in colon tissues. Professor Su-Chen Hsieh's lab has identified the bioactive compounds in COE with anti-inflammatory effects, including gallic acid (GA), ellagic acid (EA), sitoindoside I (SI), amentoflavone (AMF), and protocatechuic acid (PA). This study further investigates the regulatory effects of these compounds on intestinal barrier function and immune response. The results show that these compounds reduce COX-2 and iNOS protein levels in lipopolysaccharide (LPS)-induced RAW264.7 macrophages, decrease pro-inflammatory M1 macrophages, and increase anti-inflammatory M2 macrophages. They also improve the barrier function of the inflamed intestinal epithelial cells, CCD841, and reduce the adhesion of THP-1 monocyte to CCD841 cells. In summary, our study highlights the anti-inflammatory potential of the bioactive components in COE, which shows significant promise for protecting intestinal health, and paves the way for further research on their mechanisms and clinical applications. | en |
| dc.description.provenance | Submitted by admin ntu (admin@lib.ntu.edu.tw) on 2024-08-06T16:23:04Z No. of bitstreams: 0 | en |
| dc.description.provenance | Made available in DSpace on 2024-08-06T16:23:04Z (GMT). No. of bitstreams: 0 | en |
| dc.description.tableofcontents | 論文口試委員審定書 i
摘要 ii Abstract iii 目次 iv 圖次 vi 縮寫表 vii 一、 研究背景 1.1 發炎反應 1 1.2 發炎性腸道疾病 1.2.1 發炎性腸道疾病之簡介 3 1.2.2 現行對於 IBD 之治療 4 1.3 中國橄欖果實之生物活性與功效 5 1.4 COE 之生物活性化合物的功效研究 6 1.5 本論文之研究目的 8 二、 材料與方法 2.1 化合物 9 2.2 細胞培養基 9 2.3 細胞繼代與保存 2.3.1 細胞繼代 10 2.3.2 細胞計數 10 2.3.3 細胞冷凍保存 11 2.3.4 細胞解凍 11 2.3.5 細胞存活率分析 11 2.4 巨噬細胞 M1/M2 極化 (macrophage M1/M2 polarization) 12 2.5 腸道上皮細胞通透性 (intestinal epithelial permeability) 12 2.6 單核細胞-上皮細胞黏附實驗 (monocyte-epithelial cells adhesion assay) 13 2.7 免疫組織化學染色 (Immunohistochemistry, IHC) 13 2.8 蛋白質分析 2.8.1 細胞蛋白質萃取與定量 14 2.8.2 蛋白質膠體電泳 15 2.8.3 西方墨點法 15 2.9 RNA分析 2.9.1 RNA之純化、萃取與定量 17 2.9.2 反轉錄作用 17 2.9.3 即時定量聚合酶連鎖反應分析 (RT-qPCR) 17 三、 研究結果 3.1 COE 中的生物活性化合物對於發炎相關蛋白質含量之影響 19 3.2 COE 中的生物活性化合物對於 CCD841 細胞存活率之影響 19 3.3 COE 對於 DSS 誘導的腸炎小鼠巨噬細胞極化之影響 20 3.4 COE 中的生物活性化合物對於 THP-1 細胞 M1/M2極化之影響 21 3.5 COE 中的生物活性化合物對於發炎之 CCD841 細胞通透率之影響 22 3.6 COE 中的生物活性化合物對於 THP-1 細胞與 CCD841 細胞間附著作用之影響 22 四、 討論 24 五、 參考文獻 29 六、圖與表 39 | - |
| dc.language.iso | zh_TW | - |
| dc.subject | 腸道發炎 | zh_TW |
| dc.subject | 抗發炎 | zh_TW |
| dc.subject | 腸道屏障功能 | zh_TW |
| dc.subject | 免疫反應 | zh_TW |
| dc.subject | anti-inflammatory | en |
| dc.subject | intestinal barrier function | en |
| dc.subject | intestinal inflammation | en |
| dc.subject | immune response | en |
| dc.title | 探討中國橄欖萃取物之生物活性化合物減緩腸道發炎之機制 | zh_TW |
| dc.title | Exploring the Mechanism of Bioactive Compounds from Chinese Olive (Canarium album L.) Fruit Extract in Alleviating Intestinal Inflammation | en |
| dc.type | Thesis | - |
| dc.date.schoolyear | 112-2 | - |
| dc.description.degree | 碩士 | - |
| dc.contributor.oralexamcommittee | 謝淑貞;謝佳倩 | zh_TW |
| dc.contributor.oralexamcommittee | Shu-Chen Hsieh;Chia-Chien Hsieh | en |
| dc.subject.keyword | 腸道發炎,抗發炎,腸道屏障功能,免疫反應, | zh_TW |
| dc.subject.keyword | intestinal inflammation,anti-inflammatory,intestinal barrier function,immune response, | en |
| dc.relation.page | 57 | - |
| dc.identifier.doi | 10.6342/NTU202402200 | - |
| dc.rights.note | 未授權 | - |
| dc.date.accepted | 2024-07-28 | - |
| dc.contributor.author-college | 生命科學院 | - |
| dc.contributor.author-dept | 生化科技學系 | - |
| 顯示於系所單位: | 生化科技學系 | |
文件中的檔案:
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-112-2.pdf 未授權公開取用 | 3.56 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。
