Skip navigation

DSpace

機構典藏 DSpace 系統致力於保存各式數位資料(如:文字、圖片、PDF)並使其易於取用。

點此認識 DSpace
DSpace logo
English
中文
  • 瀏覽論文
    • 校院系所
    • 出版年
    • 作者
    • 標題
    • 關鍵字
    • 指導教授
  • 搜尋 TDR
  • 授權 Q&A
    • 我的頁面
    • 接受 E-mail 通知
    • 編輯個人資料
  1. NTU Theses and Dissertations Repository
  2. 理學院
  3. 化學系
請用此 Handle URI 來引用此文件: http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/96199
完整後設資料紀錄
DC 欄位值語言
dc.contributor.advisor劉如熹zh_TW
dc.contributor.advisorRu-Shi Liuen
dc.contributor.author王貞雅zh_TW
dc.contributor.authorChen-Ya Wangen
dc.date.accessioned2024-11-28T16:09:10Z-
dc.date.available2024-09-30-
dc.date.copyright2024-11-28-
dc.date.issued2024-
dc.date.submitted2024-09-24-
dc.identifier.citation[1] Bloem, B. R.; Okun, M. S.; Klein, C. Parkinson's Disease. Lancet 2021, 397, 2284–2303.
[2] Blagov, A.; Postnov, A.; Sukhorukov, V.; Popov, M.; Uzokov, J.; Orekhov, A. Significance of Mitochondrial Dysfunction in the Pathogenesis of Parkinson's Disease. Front. Biosci. 2024, 29, 36.
[3] Leite Silva, A. B. R.; Gonçalves de Oliveira, R. W.; Diógenes, G. P.; de Castro Aguiar, M. F.; Sallem, C. C.; Lima, M. P. P.; de Albuquerque Filho, L. B.; Peixoto de Medeiros, S. D.; Penido de Mendonça, L. L.; de Santiago Filho, P. C.; Nones, D. P.; de Silva Cardoso, P. M. M.; Ribas, M. Z.; Galvão, S. L.; Gomes, G. F.; Bezerra de Menezes, A. R.; Dos Santos, N. L.; Mororó, V. M.; Duarte, F. S.; Dos Santos, J. C. C. Premotor, Nonmotor and Motor Symptoms of Parkinson's Disease: A New Clinical State of the Art. Ageing Res. Rev. 2023, 84, 101834.
[4] Tang, Y.; Xiao, X.; Xie, H.; Wan, C. M.; Meng, L.; Liu, Z. H.; Liao, W. H.; Tang, B. S.; Guo, J. F. Altered Functional Brain Connectomes between Sporadic and Familial Parkinson's Patients. Front. Neuroanat. 2017, 11, 99.
[5] Hauser, D. N.; Hastings, T. G. Mitochondrial Dysfunction and Oxidative Stress in Parkinson's Disease and Monogenic Parkinsonism. Neurobiol. Dis. 2013, 51, 35–42.
[6] Dauer, W.; Przedborski, S. Parkinson's Disease: Mechanisms and Models. Neuron 2003, 39, 889–909.
[7] Brooker, S. M.; Naylor, G. E.; Krainc, D. Cell Biology of Parkinson's Disease: Mechanisms of Synaptic, Lysosomal, and Mitochondrial Dysfunction. Curr. Opin. Neurobiol. 2024, 85, 102841.
[8] Herman, S.; Djaldetti, R.; Mollenhauer, B.; Offen, D. Csf-Derived Extracellular Vesicles from Patients with Parkinson's Disease Induce Symptoms and Pathology. Brain 2023, 146, 209–224.
[9] Jankovic, J.; Tan, E. K. Parkinson's Disease: Etiopathogenesis and Treatment. J. Neurol. Neurosurg. Psychiatry 2020, 91, 795–808.
[10] Stojkovska, I.; Krainc, D.; Mazzulli, J. R. Molecular Mechanisms of Alpha Synuclein and GBA1 in Parkinson's Disease. Cell Tissue Res. 2018, 373, 51–60.
[11] Pozo Devoto, V. M.; Falzone, T. L. Mitochondrial Dynamics in Parkinson's Disease: A Role for Alpha-Synuclein? Dis. Model. Mech. 2017, 10, 1075–1087.
[12] Trompetero, A.; Gordillo, A.; del Pilar, M. C.; Cristina, V. M.; Bustos Cruz, R. H. Alzheimer’s Disease and Parkinson’s Disease: A Review of Current Treatment Adopting a Nanotechnology Approach. Curr. Pharm. Des. 2018, 24, 22–45.
[13] Ray, B.; Mahalakshmi, A. M.; Tuladhar, S.; Bhat, A.; Srinivasan, A.; Pellegrino, C.; Kannan, A.; Bolla, S. R.; Chidambaram, S. B.; Sakharkar, M. K. "Janus-Faced" Alpha-Synuclein: Role in Parkinson's Disease. Front. Cell. Dev. Biol. 2021, 9, 673395.
[14] De Deurwaerdère, P.; Di Giovanni, G.; Millan, M. J. Expanding the Repertoire of L-Dopa’s Actions: A Comprehensive Review of Its Functional Neurochemistry. Prog. Neurobiol. 2017, 151, 57–100.
[15] Goldenberg, M. M. Medical Management of Parkinson’s Disease. Pharm. Ther. 2008, 33, 590–606.
[16] Emamzadeh, F. N.; Surguchov, A. Parkinson's Disease: Biomarkers, Treatment, and Risk Factors. Front. Neurosci. 2018, 12, 612.
[17] Jankovic, J.; Aguilar, L. G. Current Approaches to the Treatment of Parkinson’s Disease. Neuropsychiatr. Dis. Treat. 2008, 4, 743–757.
[18] Reiter, R. J. Oxidative Processes and Antioxidative Defense Mechanisms in the Aging Brain. FASEB J. 1995, 9, 526–533.
[19] Javadov, S.; Kozlov, A. V.; Camara, A. K. S. Mitochondria in Health and Diseases. Cells 2020, 9, 1177.
[20] Perier, C.; Vila, M. Mitochondrial Biology and Parkinson's Disease. Cold Spring Harb. Perspect. Med. 2012, 2, a009332.
[21] Schapira, A. H. Mitochondrial Pathology in Parkinson's Disease. Mt. Sinai J. Med. 2011, 78, 872–881.
[22] Boyer, D. R.; Li, B.; Sun, C.; Fan, W.; Zhou, K.; Hughes, M. P.; Sawaya, M. R.; Jiang, L.; Eisenberg, D. S. The Alpha-Synuclein Hereditary Mutation E46k Unlocks a More Stable, Pathogenic Fibril Structure. Proc. Natl. Acad. Sci. U. S. A. 2020, 117, 3592–3602.
[23] Maiti, P.; Manna, J.; Dunbar, G. L. Current Understanding of the Molecular Mechanisms in Parkinson's Disease: Targets for Potential Treatments. Transl. Neurodegener. 2017, 6, 28.
[24] Kim, W. S.; Kågedal, K.; Halliday, G. M. Alpha-Synuclein Biology in Lewy Body Diseases. Alzheimer's Res. Ther. 2014, 6, 73.
[25] Marques, O.; Outeiro, T. F. Alpha-Synuclein: From Secretion to Dysfunction and Death. Cell Death Dis. 2012, 3, e350.
[26] Paillusson, S.; Gomez-Suaga, P.; Stoica, R.; Little, D.; Gissen, P.; Devine, M. J.; Noble, W.; Hanger, D. P.; Miller, C. C. J. α-Synuclein Binds to the ER-Mitochondria Tethering Protein VAPB to Disrupt Ca2+ Homeostasis and Mitochondrial ATP Production. Acta Neuropathol. 2017, 134, 129–149.
[27] Sheng, Z. H.; Cai, Q. Mitochondrial Transport in Neurons: Impact on Synaptic Homeostasis and Neurodegeneration. Nat. Rev. Neurosci. 2012, 13, 77–93.
[28] Zhang, J.; Shen, Q.; Ma, Y.; Liu, L.; Jia, W.; Chen, L.; Xie, J. Calcium Homeostasis in Parkinson's Disease: From Pathology to Treatment. Neurosci. Bull. 2022, 38, 1267–1270.
[29] Risiglione, P.; Zinghirino, F.; Di Rosa, M. C.; Magri, A.; Messina, A. Alpha Synuclein and Mitochondrial Dysfunction in Parkinson's Disease: The Emerging Role of VDAC. Biomolecules 2021, 11, 718.
[30] Weng, M.; Xie, X.; Liu, C.; Lim, K. L.; Zhang, C. W.; Li, L. The Sources of Reactive Oxygen Species and Its Possible Role in the Pathogenesis of Parkinson’s Disease. Parkinson's Dis. 2018, 2018, 9163040.
[31] Halliwell, B. Oxidative Stress and Neurodegeneration: Where Are We Now? J. Neurochem. 2006, 97, 1634–1658.
[32] Cadenas, E.; Davies, K. J. Mitochondrial Free Radical Generation, Oxidative Stress, and Aging. Free Radic. Biol. Med. 2000, 29, 222–230.
[33] Trist, B. G.; Hare, D. J.; Double, K. L. Oxidative Stress in the Aging Substantia Nigra and the Etiology of Parkinson's Disease. Aging Cell 2019, 18, e13031.
[34] Covarrubias, L.; Hernández-García, D.; Schnabel, D.; Salas-Vidal, E.; Castro Obregón, S. Function of Reactive Oxygen Species During Animal Development: Passive or Active? Dev. Biol. 2008, 320, 1–11.
[35] Manoharan, S.; Guillemin, G. J.; Abiramasundari, R. S.; Essa, M. M.; Akbar, M.; Akbar, M. D. The Role of Reactive Oxygen Species in the Pathogenesis of Alzheimer's Disease, Parkinson's Disease, and Huntington's Disease: A Mini Review. Oxidative Med. Cell. Longev. 2016, 2016, 8590578.
[36] Casetta, I.; Govoni, V.; Granieri, E. Oxidative Stress, Antioxidants and Neurodegenerative Diseases. Curr. Pharm. Des. 2005, 11, 2033–2052.
[37] Pohl, F.; Kong Thoo Lin, P. The Potential Use of Plant Natural Products and Plant Extracts with Antioxidant Properties for the Prevention/Treatment of Neurodegenerative Diseases: In Vitro, in Vivo and Clinical Trials. Molecules 2018, 23, 3283.
[38] Camilleri, A.; Vassallo, N. The Centrality of Mitochondria in the Pathogenesis and Treatment of Parkinson's Disease. CNS Neurosci. Ther. 2014, 20, 591–602.
[39] Chaturvedi, R. K.; Beal, M. F. Mitochondria Targeted Therapeutic Approaches in Parkinson's and Huntington's Diseases. Mol. Cell. Neurosci. 2013, 55, 101–114.
[40] Löhle, M.; Reichmann, H. Clinical Neuroprotection in Parkinson's Disease—Still Waiting for the Breakthrough. J. Neurol. Sci. 2010, 289, 104–114.
[41] Alshial, E. E.; Abdulghaney, M. I.; Wadan, A. S.; Abdellatif, M. A.; Ramadan, N. E.; Suleiman, A. M.; Waheed, N.; Abdellatif, M.; Mohammed, H. S. Mitochondrial Dysfunction and Neurological Disorders: A Narrative Review and Treatment Overview. Life Sci. 2023, 334, 122257.
[42] Ernster, L.; Dallner, G. Biochemical, Physiological and Medical Aspects of Ubiquinone Function. Biochim. Biophys. Acta-Mol. Basis Dis. 1995, 1271, 195–204.
[43] Moon, Y.; Lee, K. H.; Park, J. H.; Geum, D.; Kim, K. Mitochondrial Membrane Depolarization and the Selective Death of Dopaminergic Neurons by Rotenone: Protective Effect of Coenzyme Q10. J. Neurochem. 2005, 93, 1199–1208.
[44] Shults, C. W.; Oakes, D.; Kieburtz, K.; Beal, M. F.; Haas, R.; Plumb, S.; Juncos, J. L.; Nutt, J.; Shoulson, I.; Carter, J. Effects of Coenzyme Q10 in Early Parkinson Disease: Evidence of Slowing of the Functional Decline. Arch. Neurol. 2002, 59, 1541–1550.
[45] Kelso, G. F.; Porteous, C. M.; Coulter, C. V.; Hughes, G.; Porteous, W. K.; Ledgerwood, E. C.; Smith, R. A.; Murphy, M. P. Selective Targeting of a Redox-Active Ubiquinone to Mitochondria within Cells: Antioxidant and Antiapoptotic Properties. J. Biol. Chem. 2001, 276, 4588–4596.
[46] Lu, C.; Zhang, D.; Whiteman, M.; Armstrong, J. S. Is Antioxidant Potential of the Mitochondrial Targeted Ubiquinone Derivative MitoQ Conserved in Cells Lacking mtDNA? Antioxid. Redox Signal. 2008, 10, 651–660.
[47] Solesio, M. E.; Prime, T. A.; Logan, A.; Murphy, M. P.; del Mar Arroyo-Jimenez, M.; Jordán, J.; Galindo, M. F. The Mitochondria-Targeted Anti-Oxidant MitoQ Reduces Aspects of Mitochondrial Fission in the 6-OHDA Cell Model of Parkinson's Disease. Biochim. Biophys. Acta-Mol. Basis Dis. 2013, 1832, 174–182.
[48] Ghosh, A.; Chandran, K.; Kalivendi, S. V.; Joseph, J.; Antholine, W. E.; Hillard, C. J.; Kanthasamy, A.; Kanthasamy, A.; Kalyanaraman, B. Neuroprotection by a Mitochondria-Targeted Drug in a Parkinson's Disease Model. Free Radic. Biol. Med. 2010, 49, 1674–1684.
[49] Salehpour, F.; Mahmoudi, J.; Kamari, F.; Sadigh-Eteghad, S.; Rasta, S. H.; Hamblin, M. R. Brain Photobiomodulation Therapy: A Narrative Review. Mol. Neurobiol. 2018, 55, 6601–6636.
[50] Hamblin, M. R.; Waynant, R. W.; Demidova, T. N.; Anders, J. Mechanisms of Low Level Light Therapy. Proc. of SPIE 2006, 6140, 614001.
[51] Cios, A.; Cieplak, M.; Szymanski, L.; Lewicka, A.; Cierniak, S.; Stankiewicz, W.; Mendrycka, M.; Lewicki, S. Effect of Different Wavelengths of Laser Irradiation on the Skin Cells. Int. J. Mol. Sci. 2021, 22, 2437.
[52] Khamlichi, A.; Mouahid, A. Infrared Thermography Used for Composite Materials. MATEC Web Conf. 2018, 191, 00011.
[53] Hill, B. C. Modeling the Sequence of Electron Transfer Reactions in the Single Turnover of Reduced, Mammalian Cytochrome C Oxidase with Oxygen. J. Biol. Chem. 1994, 269, 2419–2425.
[54] Karu, T. Molecular Mechanism of the Therapeutic Effect of Low-Intensity Laser Radiation. Lasers Life Sci. 1988, 2, 53–74.
[55] Ball, K. A.; Castello, P. R.; Poyton, R. O. Low Intensity Light Stimulates Nitrite Dependent Nitric Oxide Synthesis but Not Oxygen Consumption by Cytochrome C Oxidase: Implications for Phototherapy. J. Photochem. Photobiol. B-Biol. 2011, 102, 182–191.
[56] Karu, T. I.; Kolyakov, S. Exact Action Spectra for Cellular Responses Relevant to Phototherapy. Photomed. Laser Surg. 2005, 23, 355–361.
[57] Santana-Blank, L.; Rodríguez-Santana, E.; Santana-Rodriguez, K. Theoretic, Experimental, Clinical Bases of the Water Oscillator Hypothesis in near-Infrared Photobiomodulation. Photomed. Laser Surg. 2010, 28, S41–S52.
[58] Hamblin, M. R. The Role of Nitric Oxide in Low Level Light Therapy. Proc. of SPIE 2008, 6846, 684602.
[59] Lu, Y.; Wang, R.; Dong, Y.; Tucker, D.; Zhao, N.; Ahmed, M. E.; Zhu, L.; Liu, T. C. Y.; Cohen, R. M.; Zhang, Q. Low-Level Laser Therapy for Beta Amyloid Toxicity in Rat Hippocampus. Neurobiol. Aging 2017, 49, 165–182.
[60] Quirk, B. J.; Torbey, M.; Buchmann, E.; Verma, S.; Whelan, H. T. Near-Infrared Photobiomodulation in an Animal Model of Traumatic Brain Injury: Improvements at the Behavioral and Biochemical Levels. Photomed. Laser Surg. 2012, 30, 523–529.
[61] Liang, H.; Whelan, H.; Eells, J.; Meng, H.; Buchmann, E.; Lerch-Gaggl, A.; Wong Riley, M. Photobiomodulation Partially Rescues Visual Cortical Neurons from Cyanide-Induced Apoptosis. Neuroscience 2006, 139, 639–649.
[62] Ando, T.; Xuan, W.; Xu, T.; Dai, T.; Sharma, S. K.; Kharkwal, G. B.; Huang, Y. Y.; Wu, Q.; Whalen, M. J.; Sato, S. Comparison of Therapeutic Effects between Pulsed and Continuous Wave 810-nm Wavelength Laser Irradiation for Traumatic Brain Injury in Mice. PLoS One 2011, 6, e26212.
[63] Yip, K.; Lo, S.; Leung, M.; So, K.; Tang, C. Y.; Poon, D. The Effect of Low-Energy Laser Irradiation on Apoptotic Factors Following Experimentally Induced Transient Cerebral Ischemia. Neuroscience 2011, 190, 301–306.
[64] De Taboada, L.; Yu, J.; El-Amouri, S.; Gattoni-Celli, S.; Richieri, S.; McCarthy, T.; Streeter, J.; Kindy, M. S. Transcranial Laser Therapy Attenuates Amyloid-Β Peptide Neuropathology in Amyloid-Β Protein Precursor Transgenic Mice. J. Alzheimer's Dis.2011, 23, 521–535.
[65] Oueslati, A.; Lovisa, B.; Perrin, J.; Wagnières, G.; van den Bergh, H.; Tardy, Y.; Lashuel, H. A. Photobiomodulation Suppresses Alpha-Synuclein-Induced Toxicity in an Aav-Based Rat Genetic Model of Parkinson’s Disease. PLoS One 2015, 10, e0140880.
[66] Marino, A.; Battaglini, M.; Moles, N.; Ciofani, G. Natural Antioxidant Compounds as Potential Pharmaceutical Tools against Neurodegenerative Diseases. ACS Omega 2022, 7, 25974–25990.
[67] Brewer, M. S. Natural Antioxidants: Sources, Compounds, Mechanisms of Action, and Potential Applications. Compr. Rev. Food. Sci. Food Saf. 2011, 10, 221–247.
[68] Kelsey, N. A.; Wilkins, H. M.; Linseman, D. A. Nutraceutical Antioxidants as Novel Neuroprotective Agents. Molecules 2010, 15, 7792–7814.
[69] Stevenson, D. E.; Hurst, R. D. Polyphenolic Phytochemicals–Just Antioxidants or Much More? Cell. Mol. Life Sci. 2007, 64, 2900–2916.
[70] Gazit, E. A Possible Role for π‐Stacking in the Self‐Assembly of Amyloid Fibrils. FASEB J. 2002, 16, 77–83.
[71] Wang, W. W.; Han, R.; He, H. J.; Li, J.; Chen, S. Y.; Gu, Y.; Xie, C. Administration of Quercetin Improves Mitochondria Quality Control and Protects the Neurons in 6-OHDA-Lesioned Parkinson's Disease Models. Aging (Albany N. Y.) 2021, 13, 11738.
[72] Ghasemzadeh Rahbardar, M.; Hosseinzadeh, H. Effects of Rosmarinic Acid on Nervous System Disorders: An Updated Review. Naunyn-Schmiedeberg's Arch. Pharmacol. 2020, 393, 1779–1795.
[73] Coelho, V. R.; Vieira, C. G.; de Souza, L. P.; da Silva, L. L.; Pflüger, P.; Regner, G. G.; Papke, D. K. M.; Picada, J. N.; Pereira, P. Behavioral and Genotoxic Evaluation of Rosmarinic and Caffeic Acid in Acute Seizure Models Induced by Pentylenetetrazole and Pilocarpine in Mice. Naunyn-Schmiedeberg's Arch. Pharmacol. 2016, 389, 1195–1203.
[74] Coelho, V. R.; Vieira, C. G.; de Souza, L. P.; Moysés, F.; Basso, C.; Papke, D. K. M.; Pires, T. R.; Siqueira, I. R.; Picada, J. N.; Pereira, P. Antiepileptogenic, Antioxidant and Genotoxic Evaluation of Rosmarinic Acid and Its Metabolite Caffeic Acid in Mice. Life Sci. 2015, 122, 65–71.
[75] Awad, R.; Muhammad, A.; Durst, T.; Trudeau, V. L.; Arnason, J. T. Bioassay‐Guided Fractionation of Lemon Balm (Melissa Officinalis L.) Using an in Vitro Measure of Gaba Transaminase Activity. Phytother. Res. 2009, 23, 1075–1081.
[76] Ono, K.; Li, L.; Takamura, Y.; Yoshiike, Y.; Zhu, L.; Han, F.; Mao, X.; Ikeda, T.; Takasaki, J. I.; Nishijo, H. Phenolic Compounds Prevent Amyloid β-Protein Oligomerization and Synaptic Dysfunction by Site-Specific Binding. J. Biol. Chem. 2012, 287, 14631–14643.
[77] Hamaguchi, T.; Ono, K.; Murase, A.; Yamada, M. Phenolic Compounds Prevent Alzheimer’s Pathology through Different Effects on the Amyloid-β Aggregation Pathway. Am. J. Pathol. 2009, 175, 2557–2565.
[78] Ono, K.; Hasegawa, K.; Naiki, H.; Yamada, M. Curcumin Has Potent Anti‐Amyloidogenic Effects for Alzheimer's β‐Amyloid Fibrils in Vitro. J. Neurosci. Res. 2004, 75, 742–750.
[79] Bhatt, R.; Singh, D.; Prakash, A.; Mishra, N. Development, Characterization and Nasal Delivery of Rosmarinic Acid-Loaded Solid Lipid Nanoparticles for the Effective Management of Huntington’s Disease. Drug Deliv. 2015, 22, 931–939.
[80] Ren, P.; Jiang, H.; Li, R.; Wang, J.; Song, N.; Xu, H. M.; Xie, J. X. Rosmarinic Acid Inhibits 6-OHDA-Induced Neurotoxicity by Anti-Oxidation in MES23.5 Cells. J. Mol. Neurosci. 2009, 39, 220–225.
[81] Lee, H. J.; Cho, H. S.; Park, E.; Kim, S.; Lee, S. Y.; Kim, C. S.; Kim, D. K.; Kim, S. J.; Chun, H. S. Rosmarinic Acid Protects Human Dopaminergic Neuronal Cells against Hydrogen Peroxide-Induced Apoptosis. Toxicology 2008, 250, 109–115.
[82] Liang, Z.; Xu, Y.; Wen, X.; Nie, H.; Hu, T.; Yang, X.; Chu, X.; Yang, J.; Deng, X.; He, J. Rosmarinic Acid Attenuates Airway Inflammation and Hyperresponsiveness in a Murine Model of Asthma. Molecules 2016, 21, 769.
[83] Fonteles, A. A.; de Souza, C. M.; de Sousa Neves, J. C.; Menezes, A. P. F.; do Carmo, M. R. S.; Fernandes, F. D. P.; de Araújo, P. R.; de Andrade, G. M. Rosmarinic Acid Prevents against Memory Deficits in Ischemic Mice. Behav. Brain Res. 2016, 297, 91–103.
[84] Tapeinos, C.; Battaglini, M.; Ciofani, G. Advances in the Design of Solid Lipid Nanoparticles and Nanostructured Lipid Carriers for Targeting Brain Diseases. J. Control. Release 2017, 264, 306–332.
[85] Uchegbu, I. F.; Vyas, S. P. Non-Ionic Surfactant Based Vesicles (Niosomes) in Drug Delivery. Int. J. Pharm. 1998, 172, 33–70.
[86] Martinelli, C.; Pucci, C.; Battaglini, M.; Marino, A.; Ciofani, G. Antioxidants and Nanotechnology: Promises and Limits of Potentially Disruptive Approaches in the Treatment of Central Nervous System Diseases. Adv. Healthc. Mater. 2020, 9, 1901589.
[87] Gullotta, G. S.; Costantino, G.; Sortino, M. A.; Spampinato, S. F. Microglia and the Blood–Brain Barrier: An External Player in Acute and Chronic Neuroinflammatory Conditions. Int. J. Mol. Sci. 2023, 24, 9144.
[88] Kong, C.; Chang, W. S. Preclinical Research on Focused Ultrasound-Mediated Blood-Brain Barrier Opening for Neurological Disorders: A Review. Neurol. Int. 2023, 15, 285–300.
[89] Pires, P. C.; Paiva-Santos, A. C.; Veiga, F. Liposome-Derived Nanosystems for the Treatment of Behavioral and Neurodegenerative Diseases: The Promise of Niosomes, Transfersomes, and Ethosomes for Increased Brain Drug Bioavailability. Pharmaceuticals 2023, 16, 1424.
[90] Seo, M. W.; Park, T. E. Recent Advances with Liposomes as Drug Carriers for Treatment of Neurodegenerative Diseases. Biomed. Eng. Lett. 2021, 11, 211–216.
[91] Kahana, M.; Weizman, A.; Gabay, M.; Loboda, Y.; Segal-Gavish, H.; Gavish, A.; Barhum, Y.; Offen, D.; Finberg, J.; Allon, N. Liposome-Based Targeting of Dopamine to the Brain: A Novel Approach for the Treatment of Parkinson’s Disease. Mol. Psychiatr. 2021, 26, 2626–2632.
[92] Cascione, M.; De Matteis, V.; Leporatti, S.; Rinaldi, R. The New Frontiers in Neurodegenerative Diseases Treatment: Liposomal-Based Strategies. Front. Bioeng. Biotechnol. 2020, 8, 566767.
[93] Wang, Z. Y.; Sreenivasmurthy, S. G.; Song, J. X.; Liu, J. Y.; Li, M. Strategies for Brain-Targeting Liposomal Delivery of Small Hydrophobic Molecules in the Treatment of Neurodegenerative Diseases. Drug Discov. Today 2019, 24, 595–605.
[94] Sokolik, V. V.; Berchenko, O. G.; Shulga, S. M. Comparative Analysis of Nasal Therapy with Soluble and Liposomal Forms of Curcumin on Rats with Alzheimer’s Disease Model. J. Alzheimer's Dis. Parkinsonism 2017, 7, 1000357.
[95] Phachonpai, W.; Wattanathorn, J.; Muchimapura, S.; Tong-Un, T.; Preechagoon, D. Neuroprotective Effect of Quercetin Encapsulated Liposomes: A Novel Therapeutic Strategy against Alzheimer's Disease. Am. J. Appl. Sci. 2010, 7, 480–485.
[96] Ghosh, A.; Mandal, A. K.; Sarkar, S.; Panda, S.; Das, N. Nanoencapsulation of Quercetin Enhances Its Dietary Efficacy in Combating Arsenic-Induced Oxidative Damage in Liver and Brain of Rats. Life Sci. 2009, 84, 75–80.
[97] Ethemoglu, M.; Seker, F.; Akkaya, H.; Kilic, E.; Aslan, I.; Erdogan, C.; Yilmaz, B. Anticonvulsant Activity of Resveratrol-Loaded Liposomes in Vivo. Neuroscience 2017, 357, 12–19.
[98] Wang, Y.; Xia, Z.; Xu, J. R.; Wang, Y. X.; Hou, L. N.; Qiu, Y.; Chen, H. Z. α Mangostin, A Polyphenolic Xanthone Derivative from Mangosteen, Attenuates β Amyloid Oligomers-Induced Neurotoxicity by Inhibiting Amyloid Aggregation. Neuropharmacology 2012, 62, 871–881.
[99] Biedler, J. L.; Roffler-Tarlov, S.; Schachner, M.; Freedman, L. S. Multiple Neurotransmitter Synthesis by Human Neuroblastoma Cell Lines and Clones. Cancer Res. 1978, 38, 3751–3757.
[100] Ross, R. A.; Biedler, J. L. Presence and Regulation of Tyrosinase Activity in Human Neuroblastoma Cell Variants in Vitro. Cancer Res. 1985, 45, 1628–1632.
[101] Nagatsu, T.; Levitt, M.; Udenfriend, S. Tyrosine Hydroxylase: The Initial Step in Norepinephrine Biosynthesis. J. Biol. Chem. 1964, 239, 2910–2917.
[102] Levin, E. Y.; Levenberg, B.; Kaufman, S. The Enzymatic Conversion of 3, 4-Dihydroxyphenylethylamine to Norepinephrine. J. Biol. Chem. 1960, 235, 2080–2086.
[103] Pandey, M.; Karmakar, V.; Majie, A.; Dwivedi, M.; Md, S.; Gorain, B. The SH SY5Y Cell Line: A Valuable Tool for Parkinson’s Disease Drug Discovery. Expert. Opin. Drug Discov. 2024, 19, 303–316.
[104] Shipley, M. M.; Mangold, C. A.; Kuny, C. V.; Szpara, M. L. Differentiated Human SH-SY5Y Cells Provide a Reductionist Model of Herpes Simplex Virus 1 Neurotropism. J. Virol. 2017, 91, e00958-17.
[105] Raza, C.; Anjum, R.; Shakeel, N. U. A. Parkinson's Disease: Mechanisms, Translational Models and Management Strategies. Life Sci. 2019, 226, 77–90.
[106] Chia, S. J.; Tan, E. K.; Chao, Y. X. Historical Perspective: Models of Parkinson's Disease. Int. J. Mol. Sci. 2020, 21, 2464.
[107] Zeng, X. S.; Geng, W. S.; Jia, J. J. Neurotoxin-Induced Animal Models of Parkinson Disease: Pathogenic Mechanism and Assessment. ASN Neuro 2018, 10, 1–15.
[108] Jagmag, S. A.; Tripathi, N.; Shukla, S. D.; Maiti, S.; Khurana, S. Evaluation of Models of Parkinson's Disease. Front. Neurosci. 2015, 9, 503.
[109] Inden, M.; Kitamura, Y.; Abe, M.; Tamaki, A.; Takata, K.; Taniguchi, T. Parkinsonian Rotenone Mouse Model: Reevaluation of Long-Term Administration of Rotenone in C57bl/6 Mice. Biol. Pharm. Bull. 2011, 34, 92–96.
[110] Sherer, T. B.; Betarbet, R.; Testa, C. M.; Seo, B. B.; Richardson, J. R.; Kim, J. H.; Miller, G. W.; Yagi, T.; Matsuno-Yagi, A.; Greenamyre, J. T. Mechanism of Toxicity in Rotenone Models of Parkinson's Disease. J. Neurosci. 2003, 23, 10756–10764.
[111] Dovonou, A.; Bolduc, C.; Soto Linan, V.; Gora, C.; Peralta Iii, M. R.; Levesque, M. Animal Models of Parkinson's Disease: Bridging the Gap between Disease Hallmarks and Research Questions. Transl. Neurodegener. 2023, 12, 36.
[112] Hastak, V.; Bandi, S.; Kashyap, S.; Singh, S.; Luqman, S.; Lodhe, M.; Peshwe, D. R.; Srivastav, A. K. Antioxidant Efficacy of Chitosan/Graphene Functionalized Superparamagnetic Iron Oxide Nanoparticles. J. Mater. Sci. Mater. Med. 2018, 29, 154.
[113] Schweizer, T.; Kubach, H.; Koch, T. Investigations to Characterize the Interactions of Light Radiation, Engine Operating Media and Fluorescence Tracers for the Use of Qualitative Light-Induced Fluorescence in Engine Systems. Automot. Engine Technol. 2021, 6, 275–287.
[114] Attoff, K.; Johansson, Y.; Cediel-Ulloa, A.; Lundqvist, J.; Gupta, R.; Caiment, F.; Gliga, A.; Forsby, A. Acrylamide Alters CREB and Retinoic Acid Signalling Pathways During Differentiation of the Human Neuroblastoma SH-SY5Y Cell Line. Sci. Rep. 2020, 10, 16714
-
dc.identifier.urihttp://tdr.lib.ntu.edu.tw/jspui/handle/123456789/96199-
dc.description.abstract隨著人口逐年老化,帕金森氏症患者數量亦隨之增加,目前無有效根治帕金森氏症之治療方法,大部分治療策略為提升多巴胺神經元中之多巴胺濃度以緩解帕金森氏症之症狀,但隨疾病症狀之發展,治療效果亦隨之逐漸下降,因目前治療策略之局限性,故需發展新治療策略以應對帕金森氏症治療之挑戰。
本研究提出帕金森氏症之新治療方式,開發奈米微脂體複合迷迭香酸之奈米藥物材料,亦結合近紅外光之光生物調節治療,此方法藉具抗氧化性之天然藥物迷迭香酸抑制活性氧化物質之產生,藉微脂體包覆天然藥物可增加藥物穩定度、藥物遞送率及生物利用度,而藉粒線體複合物 IV 於近紅外光之吸收,增強電子傳遞鏈之遞送,增加三磷酸腺苷之生成,以抑制細胞之凋亡,本研究藉開發之奈米微脂體複合迷迭香酸、近紅外光及奈米微脂體複合迷迭香酸結合近紅外光之治療方式,應用於魚藤酮誘導之帕金森氏症細胞模型,探討方法於帕金森氏症治療之可行性。
本研究提出之奈米微脂體複合迷迭香酸之藥物治療結合近紅外光之光生物調節治療方式於魚藤酮誘導之帕金森模型具最高21%之恢復率,此方法結合奈米微脂體複合迷迭香酸之抗氧化治療與近紅外光之光生物調節治療,兩者結合使恢復率增加,表明此方式具治療帕金森氏症之潛力。
zh_TW
dc.description.abstractAs the population ages, the number of Parkinson's disease patients increases, and there is no effective cure. Most treatments aim to increase dopamine levels to relieve symptoms, but their effectiveness decreases as the disease progresses. Therefore, new treatment strategies are needed.
This study proposes a new treatment for Parkinson's disease by developing a nanodrug material composed of liposome complexes with rosmarinic acid and combined with near-infrared (NIR) photobiomodulation therapy. This method utilizes the antioxidant properties of the rosmarinic acid to inhibit the production of reactive oxygen species. Encapsulating the natural drug in liposomes increases the stability, delivery rate, and bioavailability. Additionally, the absorption of NIR by mitochondrial complex IV enhances electron transport chain activity, increasing adenosine triphosphate production and inhibiting cell apoptosis. This study explores the feasibility of this approach by applying the developed nano-liposome complex with rosmarinic acid, NIR, and their combination to a rotenone-induced Parkinson's disease cell model.
The proposed treatment method, combining nano-liposome complex with rosmarinic acid and near-infrared photobiomodulation therapy shows a 21% recovery rate in the rotenone-induced Parkinson's disease model. This method combines the antioxidant treatment of the nano-liposome complex with rosmarinic acid and the photobiomodulation treatment of NIR, resulting in an increased recovery rate, indicating its potential as a therapeutic approach for Parkinson's disease.
en
dc.description.provenanceSubmitted by admin ntu (admin@lib.ntu.edu.tw) on 2024-11-28T16:09:10Z
No. of bitstreams: 0
en
dc.description.provenanceMade available in DSpace on 2024-11-28T16:09:10Z (GMT). No. of bitstreams: 0en
dc.description.tableofcontents口試委員審定書........... I
誌謝...........II
摘要...........III
ABSTRACT...........IV
目次...........V
圖次...........X
表次............XIV
英文縮寫表...... XV
第一章 緒論.............1
1.1 帕金森氏症之簡介.......1
1.1.1 帕金森氏症之成因.....2
1.1.2 帕金森氏症之治療.....4
1.2 粒線體之簡介...........6
1.2.1 粒線體之生理作用.....7
1.2.2 粒線體失能與帕金森氏症........8
1.2.3 粒線體失能之帕金森氏症治療....12
1.3 光生物調節...............13
1.3.1 近紅外光之生物應用...16
1.4 天然化合物之簡介..........18
1.4.1 天然化合物之醫學應用.....19
1.4.2 迷迭香酸之簡介............20
1.4.3 迷迭香酸之生理調節機制....21
1.4.4 迷迭香酸與腦部疾病治療....22
1.5 奈米藥物載體之簡介........23
1.5.1 血腦屏障................24
1.5.2 微脂體之遞送機制.........26
1.5.3 微脂體與腦部疾病治療.....27
1.6 帕金森氏症細胞模型..........28
1.6.1 魚藤酮之生理調節..........31
1.7 研究動機與目的...............32
第二章 實驗步驟與儀器分析原理...33
2.1 化學藥品.....................33
2.2 實驗步驟...........35
2.2.1 材料合成................35
2.2.1.1 奈米微脂體之合成..........35
2.2.1.2 奈米微脂體複合迷迭香酸之合成.......36
2.2.2 材料鑑定....................37
2.2.2.1 負染色法樣品配製...........37
2.2.2.2 穩定性測試...............38
2.2.2.3 1,1-二苯基-2-三硝基苯肼之抗氧化測試......38
2.2.2.4 包覆效率與負載濃度測試.......39
2.2.3 細胞實驗.............40
2.2.3.1 細胞之培養.......40
2.2.3.2 細胞分化.......40
2.2.3.3 奈米微脂體複合迷迭香酸之細胞相容性測試......41
2.2.3.3.1 奈米微脂體複合迷迭香酸之細胞相容性測試.......41
2.2.3.3.2 近紅外光發光二極體之細胞相容性測試...........41
2.2.3.3.3 奈米微脂體複合迷迭香酸結合近紅外光發光二極體之細胞相容性測...42
2.2.3.4 帕金森氏症細胞模型建立....43
2.2.3.5 帕金森氏症細胞之研究..........44
2.2.3.5.1 奈米微脂體複合迷迭香酸於帕金森氏症細胞之研究....44
2.2.3.5.2 近紅外光發光二極體於帕金森氏症細胞之作用.........44
2.2.3.5.3 奈米微脂體複合迷迭香酸結合近紅外光發光二極體於帕金森氏症細胞之研究...45
2.2.3.6 粒線體膜電位分析(JC-10 assay)..................46
2.2.3.7 超氧化物歧化酶活性分析(Superoxide dismutase assay)........48
2.2.3.8 流式細胞儀量測(Flow cytometry)........................49
2.2.3.9 共軛焦雷射掃描顯微鏡(Confocal laser scanning microscopy; CLSM)....50
2.3 儀器原理.....................50
2.3.1 材料合成.............................50
2.3.1.1 超音波均質機(Sonicator)...50
2.3.2 材料鑑定................51
2.3.2.1 穿透式電子顯微鏡(transmission electron microscope; TEM)......51
2.3.2.2 紫外光/可見光吸收光譜儀(Ultraviolet visible spectrophotometer; UV-Vis)......53
2.3.2.3 光激發光譜儀(Photoluminescence spectrometer; PL) ......54
2.3.2.4 奈米粒徑與界達電位量測儀 (Dynamic light scattering and zeta potential analyzer; DLS)......55
2.3.3 細胞實驗..............57
2.3.3.1 多模式吸收與螢光光譜儀(Hybrid multi-mode microplate reader)........57
2.3.3.2 流式細胞儀(Flow cytometry).........58
2.3.3.3 共軛焦雷射掃描顯微鏡(Confocal laser scanning microscopy; CLSM).....59
第三章 結果與討論.........61
3.1 合成材料之鑑定.........61
3.1.1 形貌鑑定.........61
3.1.2 光學性質分析...........62
3.1.3 粒徑大小與表面電位分析............63
3.1.4 穩定性測試............65
3.1.5 1,1-二苯基-2-三硝基苯肼之抗氧化能力結果分析.......67
3.1.6 奈米微脂體複合迷迭香酸之包覆率與負載濃度之探討....68
3.2 細胞實驗............70
3.2.1 細胞分化前後之形貌分析.........70
3.2.2 細胞相容性分析...........71
3.2.2.1 迷迭香酸與奈米微脂體複合迷迭香酸之細胞相容性測試....71
3.2.2.2 近紅外光發光二極體之細胞相容性測試.....72
3.2.2.3 奈米微脂體複合迷迭香酸結合近紅外光發光二極體之細胞相容性測試..73
3.2.3 魚藤酮之細胞毒殺率分析........74
3.2.4 帕金森氏症細胞存活率分析......75
3.2.4.1 迷迭香酸與奈米微脂體複合迷迭香酸之帕金森氏症細胞存活率分析.....75
3.2.4.2 近紅外光發光二極體之帕金森氏症細胞存活率分析.......................77
3.2.4.3 奈米微脂體複合迷迭香酸結合近紅外光發光二極體之帕金森氏症細胞存活率分析....78
3.2.5 粒線體膜電位分析............79
3.2.6 超氧化物歧化酶活性分析........80
3.2.7 共軛焦顯微鏡影像結果分析......85
3.2.8 流式細胞儀結果分析............87
第四章 結論...........91
參考文獻........92
-
dc.language.isozh_TW-
dc.subject微脂體zh_TW
dc.subject光生物調節zh_TW
dc.subject帕金森氏症zh_TW
dc.subject近紅外光zh_TW
dc.subject天然化合物zh_TW
dc.subject迷迭香酸zh_TW
dc.subjectnatural compoundsen
dc.subjectParkinson's diseaseen
dc.subjectliposomesen
dc.subjectphotobiomodulationen
dc.subjectrosmarinic aciden
dc.subjectnear-infrareden
dc.title結合奈米微脂體複合迷迭香酸與近紅外線光於帕金森氏症之研究zh_TW
dc.titleResearch on Combining Nano-liposome Complex of Rosmarinic Acid with Near-infrared Light for Parkinson's Diseaseen
dc.typeThesis-
dc.date.schoolyear113-1-
dc.description.degree碩士-
dc.contributor.oralexamcommittee方俊民;朱忠瀚;鍾仁傑;詹明賢zh_TW
dc.contributor.oralexamcommitteeJim-Min Fang;John Chu;Ren-Jei Chung;Ming-Hsien Chanen
dc.subject.keyword帕金森氏症,微脂體,光生物調節,迷迭香酸,近紅外光,天然化合物,zh_TW
dc.subject.keywordParkinson's disease,liposomes,photobiomodulation,rosmarinic acid,near-infrared,natural compounds,en
dc.relation.page105-
dc.identifier.doi10.6342/NTU202403723-
dc.rights.note同意授權(限校園內公開)-
dc.date.accepted2024-09-24-
dc.contributor.author-college理學院-
dc.contributor.author-dept化學系-
dc.date.embargo-lift2029-09-09-
顯示於系所單位:化學系

文件中的檔案:
檔案 大小格式 
ntu-113-1.pdf
  未授權公開取用
5.82 MBAdobe PDF檢視/開啟
顯示文件簡單紀錄


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。

社群連結
聯絡資訊
10617臺北市大安區羅斯福路四段1號
No.1 Sec.4, Roosevelt Rd., Taipei, Taiwan, R.O.C. 106
Tel: (02)33662353
Email: ntuetds@ntu.edu.tw
意見箱
相關連結
館藏目錄
國內圖書館整合查詢 MetaCat
臺大學術典藏 NTU Scholars
臺大圖書館數位典藏館
本站聲明
© NTU Library All Rights Reserved