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???org.dspace.app.webui.jsptag.ItemTag.dcfield??? | Value | Language |
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dc.contributor.advisor | 潘建源(Chien-Yuan Pan) | |
dc.contributor.author | Hung-Lun Chen | en |
dc.contributor.author | 陳泓綸 | zh_TW |
dc.date.accessioned | 2021-06-16T10:18:58Z | - |
dc.date.available | 2013-09-24 | |
dc.date.copyright | 2013-09-24 | |
dc.date.issued | 2013 | |
dc.date.submitted | 2013-08-16 | |
dc.identifier.citation | Akopian, A.N., Souslova, V., England, S., Okuse, K., Ogata, N., Ure, J., Smith, A., Kerr, B.J., McMahon, S.B., Boyce, S., et al. (1999). The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways. Nature Neuroscience 2, 541-548.
Beckh, S., Noda, M., Lubbert, H., and Numa, S. (1989). Differential subcellular localization of the RI and RII Na+ channel subtypes in central neurons. Embo Journal 8, 3611-3616. Benzie, I.F.F., Szeto, Y.T., Strain, J.J., and Tomlinson, B. (1999). Consumption of green tea causes rapid increase in plasma antioxidant power in humans. Nutrition and Cancer-an International Journal 34, 83-87. Bouhours, M., Sternberg, D., Davoine, C.S., Ferrer, X., Willer, J.C., Fontaine, B., and Tabti, N. (2004). Functional characterization and cold sensitivity of T1313A, a new mutation of the skeletal muscle sodium channel causing paramyotonia congenita in humans. Journal of Physiology-London 554, 635-647. Burton, G., and Wayner, D.D.M. (1985). FREE-RADICALS IN BIOLOGY AND MEDICINE - HALLIWELL,B, GUTTERIDGE,JMC. Nature 318, 322-322. Cabrera, C., Artacho, R., and Gimenez, R. (2006). Beneficial effects of green tea--a review. Journal of the American College of Nutrition 25, 79-99. Cabrera, C., Gimenez, R., and Lopez, M.C. (2003). Determination of tea components with antioxidant activity. Journal of Agricultural and Food Chemistry 51, 4427-4435. Catterall, W.A. (2000). From ionic currents to molecular mechanisms: The structure and function of voltage-gated sodium channels. Neuron 26, 13-25. Chacko, S.M., Thambi, P.T., Kuttan, R., and Nishigaki, I. (2010). Beneficial effects of green tea: a literature review. Chinese medicine 5, 13. Chahine, M., George, A.L., Zhou, M., Ji, S., Sun, W.J., Barchi, R.L., and Horn, R. (1994). Sodium channel mutations in paramyotonia congenita uncouple inactivation from activation. Neuron 12, 281-294. Choi, J.Y., Park, C.S., Kim, D.J., Cho, M.H., Jin, B.K., Pie, J.E., and Chung, W.G. (2002). Prevention of nitric oxide-mediated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's disease in mice by tea phenolic epigallocatechin 3-gallate. Neurotoxicology 23, 367-374. Chung, J.H., Han, J.H., Hwang, E.J., Seo, J.Y., Cho, K.H., Kim, K.H., Youn, J.I., and Eun, H.C. (2003). Dual mechanisms of green tea extract-induced cell survival in human epidermal keratinocytes. Faseb Journal 17, 1913-+. Chyu, K.Y., Babbidge, S.M., Zhao, X.N., Dandillaya, R., Rietveld, A.G., Yano, J., Dimayuga, P., Cercek, B., and Shah, P.K. (2004). Differential effects of green tea-derived catechin on developing versus established atherosclerosis in apolipoprotein E-null mice. Circulation 109, 2448-2453. Cusdin, F.S., Clare, J.J., and Jackson, A.P. (2008). Trafficking and cellular distribution of voltage-gated sodium channels. Traffic 9, 17-26. Deng, H.M., Yin, S.T., Yan, D., Tang, M.L., Li, C.C., Chen, J.T., Wang, M., and Ruan, D.Y. (2008). Effects of EGCG on voltage-gated sodium channels in primary cultures of rat hippocampal CA1 neurons. Toxicology 252, 1-8. Goldin, A.L. (2001). Resurgence of sodium channel research. Annual Review of Physiology 63, 871-894. Gouni-Berthold, I., and Sachinidis, A. (2004). Molecular mechanisms explaining the preventive effects of catechins on the development of proliferative diseases. Current Pharmaceutical Design 10, 1261-1271. Guy, H.R., and Seetharamulu, P. (1986). MOLECULAR-MODEL OF THE ACTION-POTENTIAL SODIUM-CHANNEL. Proceedings of the National Academy of Sciences of the United States of America 83, 508-512. Hastak, K., Gupta, S., Ahmad, N., Agarwal, M.K., Agarwal, M.L., and Mukhtar, H. (2003). Role of p53 and NF-kappa B in epigallocatechin-3-gallate-induced apoptosis of LNCaP cells. Oncogene 22, 4851-4859. Hodgkin, A.L., and Huxley, A.F. (1952). A quantitative description of membrane current and its application to conduction and excitation in nerve. The Journal of physiology 117, 500-544. Jarecki, B.W., Piekarz, A.D., Jackson, J.O., II, and Cummins, T.R. (2010). Human voltage-gated sodium channel mutations that cause inherited neuronal and muscle channelopathies increase resurgent sodium currents. Journal of Clinical Investigation 120, 369-378. Jeong, H.S., Jang, S., Jang, M.J., Lee, S.G., Kim, T.S., Tag, H., Lee, J.H., Jun, J.Y., and Park, J.S. (2007). Effects of (-)-epigallocatechin-3-gallate on the activity of substantia nigra dopaminergic neurons. Brain research 1130, 114-118. Jung, H.Y., Mickus, T., and Spruston, N. (1997). Prolonged sodium channel inactivation contributes to dendritic action potential attenuation in hippocampal pyramidal neurons. Journal of Neuroscience 17, 6639-6646. Kang, J., Cheng, H., Ji, J., Incardona, J., and Rampe, D. (2010). In vitro electrocardiographic and cardiac ion channel effects of (-)-epigallocatechin-3-gallate, the main catechin of green tea. The Journal of pharmacology and experimental therapeutics 334, 619-626. Kim, T.H., Lim, J.M., Kim, S.S., Kim, J., Park, M., and Song, J.H. (2009). Effects of (-) epigallocatechin-3-gallate on Na(+) currents in rat dorsal root ganglion neurons. European journal of pharmacology 604, 20-26. Klaunig, J.E., Xu, Y., Han, C., Kamendulis, L.M., Chen, J.S., Heiser, C., Gordon, M.S., and Mohler, E.R. (1999). The effect of tea consumption on oxidative stress in smokers and nonsmokers. Proceedings of the Society for Experimental Biology and Medicine 220, 249-254. Leenen, R., Roodenburg, A.J.C., Tijburg, L.B.M., and Wiseman, S.A. (2000). A single dose of tea with or without milk increases plasma antioxidant activity in humans. European Journal of Clinical Nutrition 54, 87-92. Levites, Y., Amit, T., Mandel, S., and Youdim, M.B.H. (2003). Neuroprotection and neurorescue against A beta toxicity and PKC-dependent release of non-amyloidogenic soluble precursor protein by green tea polyphenol (-)-epigallocatechin-3-gallate. Faseb Journal 17, 952-+. Levites, Y., Amit, T., Youdim, M.B.H., and Mandel, S. (2002). Involvement of protein kinase C activation and cell survival/cell cycle genes in green tea polyphenol (-)-epigallocatechin 3-gallate neuroprotective action. Journal of Biological Chemistry 277, 30574-30580. Levites, Y., Weinreb, O., Maor, G., Youdim, M.B., and Mandel, S. (2001). Green tea polyphenol (-)-epigallocatechin-3-gallate prevents N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced dopaminergic neurodegeneration. Journal of neurochemistry 78, 1073-1082. Malhotra, J.D., Kazen-Gillespie, K., Hortsch, M., and Isom, L.L. (2000). Sodium channel beta subunits mediate homophilic cell adhesion and recruit ankyrin to points of cell-cell contact. Journal of Biological Chemistry 275, 11383-11388. Mandel, S., Weinreb, O., Amit, T., and Youdim, M.B.H. (2004). Cell signaling pathways in the neuroprotective actions of the green tea polyphenol (-)-epigallocatechin-3-gallate: implications for neurodegenerative diseases. Journal of Neurochemistry 88, 1555-1569. McKay, D.L., and Blumberg, J.B. (2002). The role of tea in human health: an update. Journal of the American College of Nutrition 21, 1-13. Mitrovic, N., George, A.L., Lerche, H., Wagner, S., Fahlke, C., and Lehmannhorn, F. (1995). Different effects on gating of three myotonia-causing mutations in the inactivation gate of the human muscle sodium channel. Journal of Physiology-London 487, 107-114. Nakagawa, K., Okuda, S., and Miyazawa, T. (1997). Dose-dependent incorporation of tea catechins, (-)-epigallocatechin-3-gallate and (-)-epigallocatechin, into human plasma. Bioscience, biotechnology, and biochemistry 61, 1981-1985. Negishi, H., Xu, J.W., Ikeda, K., Njelekela, M., Nara, Y., and Yamori, Y. (2004). Black and green tea polyphenols attenuate blood pressure increases in stroke-prone spontaneously hypertensive rats. Journal of Nutrition 134, 38-42. Noda, M., Shimizu, S., Tanabe, T., Takai, T., Kayano, T., Ikeda, T., Takahashi, H., Nakayama, H., Kanaoka, Y., Minamino, N., et al. (1984). PRIMARY STRUCTURE OF ELECTROPHORUS-ELECTRICUS SODIUM-CHANNEL DEDUCED FROM CDNA SEQUENCE. Nature 312, 121-127. Pan, C.Y., Kao, Y.H., and Fox, A.P. (2002). Enhancement of inward Ca2+ currents in bovine chrornaffin cells by green tea polyphenol extracts. Neurochemistry International 40, 131-137. Rietveld, A., and Wiseman, S. (2003). Antioxidant effects of tea: Evidence from human clinical trials. Journal of Nutrition 133, 3285S-3292S. Salah, N., Miller, N.J., Paganga, G., Tijburg, L., Bolwell, G.P., and Riceevans, C. (1995). Polypenolic flavanols as scavengers of aqueous-phase radicals and as chain-breaking antioxidants. Archives of Biochemistry and Biophysics 322, 339-346. Sano, J., Inami, S., Seimiya, K., Ohba, T., Sakai, S., Takano, T., and Mizuno, K. (2004). Effects of green tea intake on the development of coronary artery disease. Circulation Journal 68, 665-670. Suganuma, M., Okabe, S., Oniyama, M., Tada, Y., Ito, H., and Fujiki, H. (1998). Wide distribution of [3H](-)-epigallocatechin gallate, a cancer preventive tea polyphenol, in mouse tissue. Carcinogenesis 19, 1771-1776. ToledoAral, J.J., Moss, B.L., He, Z.J., Koszowski, A.G., Whisenand, T., Levinson, S.R., Wolf, J.J., SilosSantiago, I., Halegoua, S., and Mandel, G. (1997). Identification of PN1, a predominant voltage-dependent sodium channel expressed principally in peripheral neurons. Proceedings of the National Academy of Sciences of the United States of America 94, 1527-1532. Tsuneki, H., Ishizuka, M., Terasawa, M., Wu, J.-B., Sasaoka, T., and Kimura, I. (2004). Effect of green tea on blood glucose levels and serum proteomic patterns in diabetic (db/db) mice and on glucose metabolism in healthy humans. BMC Pharmacology 4, 18. van Acker, S., van Balen, G.P., van den Berg, D.J., Bast, A., and van der Vijgh, W.J.F. (1998). Influence of iron chelation on the antioxidant activity of flavonoids. Biochemical Pharmacology 56, 935-943. Van Amelsvoort, J.M.M., Hof, K.H.V., Mathot, J., Mulder, T.P.J., Wiersma, A., and Tijburg, L.B.M. (2001). Plasma concentrations of individual tea catechins after a single oral dose in humans. Xenobiotica 31, 891-901. Venance, S.L., Cannon, S.C., Fialho, D., Fontaine, B., Hanna, M.G., Ptacek, L.J., Tristani-Firouzi, M., Tawil, R., Griggs, R.C., and investigators, C. (2006). The primary periodic paralyses: diagnosis, pathogenesis and treatment. Brain 129, 8-17. Vinson, J.A., Dabbagh, Y.A., Serry, M.M., and Jang, J.H. (1995). PLANT FLAVONOIDS, ESPECIALLY TEA FLAVONOLS, ARE POWERFUL ANTIOXIDANTS USING AN IN-VITRO OXIDATION MODEL FOR HEART-DISEASE. Journal of Agricultural and Food Chemistry 43, 2800-2802. Waltner-Law, M.E., Wang, X.H.L., Law, B.K., Hall, R.K., Nawano, M., and Granner, D.K. (2002). Epigallocatechin gallate, a constituent of green tea, represses hepatic glucose production. Journal of Biological Chemistry 277, 34933-34940. Weber, J.M., Ruzindana-Umunyana, A., Imbeault, L., and Sircar, S. (2003). Inhibition of adenovirus infection and adenain by green tea catechins. Antiviral Research 58, 167-173. Weinreb, O., Mandel, S., Amit, T., and Youdim, M.B.H. (2004). Neurological mechanisms of green tea polyphenols in Alzheimer's and Parkinson's diseases. Journal of Nutritional Biochemistry 15, 506-516. Westenbroek, R.E., Merrick, D.K., and Catterall, W.A. (1989). Differential subcellular localization of the RI and RII Na+ channel subtypes in central neurons. Neuron 3, 695-704. Whitaker, W.R.J., Faull, R.L.M., Waldvogel, H.J., Plumpton, C.J., Emson, P.C., and Jeffrey, J.J. (2001). Comparative distribution of voltage-gated sodium channel proteins in human brain. Molecular Brain Research 88, 37-53. Wu, A.Z.Y., Loh, S.H., Cheng, T.H., Lu, H.H., and Lin, C.I. (2013). Antiarrhythmic effects of (-)-epicatechin-3-gallate, a novel sodium channel agonist in cultured neonatal rat ventricular myocytes. Biochemical pharmacology 85, 69-80. Yam, T.S., Shah, S., and HamiltonMiller, J.M.T. (1997). Microbiological activity of whole and fractionated crude extracts of tea (Camellia sinensis), and of tea components. Fems Microbiology Letters 152, 169-174. Yang, C.S., Chen, L.S., Lee, M.J., Balentine, D., Kuo, M.C., and Schantz, S.P. (1998). Blood and urine levels of tea catechins after ingestion of different amounts of green tea by human volunteers. Cancer Epidemiology Biomarkers & Prevention 7, 351-354. Yang, N.B., George, A.L., and Horn, R. (1997). Probing the outer vestibule of a sodium channel voltage sensor. Biophys J 73, 2260-2268. Yang, N.B., and Horn, R. (1995). EVIDENCE FOR VOLTAGE-DEPENDENT S4 MOVEMENT IN SODIUM-CHANNELS. Neuron 15, 213-218. Yee, Y.K., Koo, M.W.L., and Szeto, M.L. (2002). Chinese tea consumption and lower risk of Helicobacter infection. Journal of Gastroenterology and Hepatology 17, 552-555. Yu, E.J., Ko, S.H., Lenkowski, P.W., Pance, A., Patel, M.K., and Jackson, A.P. (2005). Distinct domains of the sodium channel beta 3-subunit modulate channel-gating kinetics and subcellular location. Biochemical Journal 392, 519-526. Yu, F.H., Westenbroek, R.E., Silos-Santiago, I., McCormick, K.A., Lawson, D., Ge, P., Ferriera, H., Lilly, J., DiStefano, P.S., Catterall, W.A., et al. (2003). Sodium channel beta 4, a new disulfide-linked auxiliary subunit with similarity to beta 2. Journal of Neuroscience 23, 7577-7585. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/60467 | - |
dc.description.abstract | 飲用綠茶對健康有許多益處,並且可以提振我們的精神。在試管和活體內的實驗已經證實兒茶素具有對抗氧化傷害的能力,並且會影響和細胞存活與細胞死亡有關的訊息傳遞途徑。除此之外,也發現 (-)-epigallocatechin-3-gallate (ECGC)具有抗癌症發生、抗高血壓以及降低心血管疾病發生風險的功效。更進一步地,EGCG和 (-)-epicatechin-3-gallate (ECG)也被發現會藉由調控離子通道的活性來影響神經的活性,尤其是藉由電壓閥鈉離子通道(VGSC)來調控。為了驗證兒茶素如何調控電壓閥鈉離子通道,我們對初級培養大鼠胚胎神經細胞和表現第四型電壓閥鈉離子通道(Nav1.4)的HEK 293T細胞使用全細胞模式的膜片箝制技術,並在施加ECG (30 μM)前後分別記錄細胞的鈉離子電流。我們的結果顯示ECG會減慢神經細胞鈉離子電流的衰退,但並不會影響神經細胞中VGSC的電壓依賴性的開關機制。施加ECG會使神經細胞中VGSC的不活化曲線往較負的電壓方向位移,並且會讓從不活化狀態回復到關閉狀態的比例下降。另外,ECG會減慢Nav1.4的電流衰退,並且會使離子通道的活化曲線往更低的電壓平移。ECG也會使Nav1.4的不活化曲線往較正的電壓方向位移,並且減低在從不活化狀態回復到關閉狀態的比例。再來,為了研究ECG會對神經細胞的突觸傳導造成什麼影響,我們施用Fluo-2來做胞內鈣離子的指示劑,並用波長為405 nm的雷射光活化MNI-glutamate來刺激目標神經細胞。初步的結果顯示,ECG可能對皮質神經細胞的突觸傳導有抑制的效果。這些結果指出一些關於ECG的新進展,包括ECG對VGSC的調控以及ECG會對VGSC不同表現型的動力學有不同的影響。 | zh_TW |
dc.description.abstract | Consuming green tea refreshes the mind and provides many health benefits. Catechins have the ability against the oxidative damages in vitro and in vivo, and their effects on signal transduction pathways are associated with cell death and cell survival. Besides, (-)-epigallocatechin-3-gallate (ECGC) has the effects as anti-carcinogenesis, anti-hypertension, and lowering cardiovascular disease risk. Furthermore, EGCG and (-)-epicatechin-3-gallate (ECG) have effects on neural activities by modulating the ion channel activities, especially the voltage-gated sodium channels (VGSCs). To verify how catechins modulate the VGSC activities, primary cultured embryonic cortical neurons and HEK 293T cells which expressed Na(v)1.4 were patch-clamped in whole-cell mode, and sodium currents were recorded before and after ECG (30 μM) treatment. Our results suggested ECG slows the slow decay of neuronal sodium currents, whereas ECG did not alter the voltage-dependence activation of neuronal VGSCs. ECG shifts the inactivation curve negatively and lengthens the recovery from inactivation. Besides, ECG slows the decay of Na(v)1.4 current, and shifts the activation curve towards negative voltage. ECG shifts the inactivation curve positively and reduces the steady-state recovery of Na(v)1.4. To investigate how ECG affects the synaptic transmission in neuron, we applied the Fluo-2, a calcium dye, and MNI-glutamate to stimulate the target neuron locally by 405-nm laser. The preliminary results suggested that ECG may have an inhibitory effect on synaptic transmission in cortical neurons. These findings reveal the new knowledge about the modulation of ECG on VGSC, and ECG has different effects on kinetics of different VGSC subtypes. | en |
dc.description.provenance | Made available in DSpace on 2021-06-16T10:18:58Z (GMT). No. of bitstreams: 1 ntu-102-R00454004-1.pdf: 2975150 bytes, checksum: b975436f1b1abfb2468881947ef88d9d (MD5) Previous issue date: 2013 | en |
dc.description.tableofcontents | 致謝 iii
摘要 iv Abstract v Introduction 1 The chemical components of green tea 1 The bioavailability and metabolism of green tea catechins 2 Molecular mechanisms of green tea catechins effects 3 The health benefits of green tea catechins 7 The electrophysiological effects of catechins 8 The structure of voltage-gated sodium cahnnels (VGSCs) 9 The expression patterns and functions of VGSC subtypes 11 The relationship of VGSCs to sodium currents and action potential 12 Channelopathies caused by mutations in Nav1.4 13 Aims 15 Materials and Methods 16 Chemicals 16 Plasmids 16 Competent Cell preparation 16 Transformation 17 Primary embryonic neuronal cell culture 17 HEK 293T cell culture 18 Transfection 19 Pipette solution 19 Bath buffer 19 Electrophysiology 20 Data acquirement and analysis 20 Calcium image of neuronal cells 22 Results 24 ECG slows the decay rate of neuronal sodium currents 24 ECG shifts the inactivation curve towards negative voltage 25 ECG lengthens the recovery from inactivation in neurons 26 ECG slows the Nav1.4 current decay 27 ECG alters the voltage-dependent activation of Nav1.4 28 ECG shifts the inactivation curve of Nav1.4 towards positive voltage 28 ECG delays the recovery from inactivation 29 ECG may inhibit the synaptic transmission 29 Discussion 31 ECG probably affects the inactivation gating of neuronal VGSC 31 ECG is likely to stabilize O state of Nav1.4 and retard the inactivation gating 33 Comparisons with effects of EGCG on the kinetics of neuronal VGSC 35 Comparisons with effects of channelopathies 35 Potential effects of ECG on synaptic transmission 36 References 37 Figure 1. Representative whole-cell currents of primary cultured embryonic cortical neurons. 47 Figure 2. ECG does not alter the current-voltage relationship. 48 Figure 3. ECG slows the decay rate of the elicited neuronal sodium currents. 49 Figure 4. ECG does not alter the voltage dependent activation of VGSCs. 50 Figure 5. ECG shifts the inactivation curve towards negative voltage. 51 Figure 6. ECG lengthens the recovery from inactivation. 52 Figure 7. Representative traces of the Nav1.4 currents in 293T cells. 53 Figure 8. ECG does not alter current-voltage relationship of Nav1.4. 54 Figure 9. ECG slows the decay rate of Nav1.4 currents 55 Figure 10. ECG alters the voltage dependent activation of Nav1.4. 56 Figure 11. ECG shifts the inactivation curve of Nav1.4 towards positive voltage. 57 Figure 12. ECG treatment elevates the potential required to inactive the Nav1.4. 58 Figure 13. ECG delays the recovery from inactivation. 59 Figure 14. Representative calcium images in primary cultured cortical neurons. 60 Figure 15. Calcium responses evoked by glutamate in primary cultured cortical neurons. 61 Figure 16. ECG may inhibit the synaptic transmission. 62 | |
dc.language.iso | en | |
dc.title | (-)-Epicatechin-3-gallate對第四型電壓閥鈉離子通道與初級培養大鼠胚胎神經細胞電流的影響 | zh_TW |
dc.title | Effects of (-)-Epicatechin-3-gallate on the currents of Na(v)1.4 and Primary Cultured Embryonic Cortical Neurons | en |
dc.type | Thesis | |
dc.date.schoolyear | 101-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 郭鐘金(Chung-Chin Kuo),王致恬(Chih-Tien Wang),蔣丙煌(Been-Huang Chiang) | |
dc.subject.keyword | (-)-epicatechin-3-gallate (ECG),電壓閥鈉離子通道,突觸傳導,電壓依賴性的開關機制,從不活化狀態到關閉狀態的回復,穩定的不活化狀態, | zh_TW |
dc.subject.keyword | (-)-epicatechin-3-gallate (ECG),voltage-gated sodium channels (VGSCs),synaptic transmission,voltage-dependence activation,recovery from inactivation,steady-state inactivation, | en |
dc.relation.page | 62 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2013-08-16 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 腦與心智科學研究所 | zh_TW |
Appears in Collections: | 腦與心智科學研究所 |
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