Yu, Siu Lung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 117-124). / Abstracts in English and Chinese. / Acknowledgements --- p.i / Abstract --- p.ii / Chinese Abstract --- p.iv / Table of Contents --- p.v / List of Figures --- p.viii / List of Tables --- p.x / List of Abbreviations --- p.xi / Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- General introduction of sleep --- p.1 / Chapter 1.1.1 --- Sleep disorders --- p.1 / Chapter 1.1.2 --- Classification systems for sleep disorders --- p.2 / Chapter 1.2 --- Insomnia --- p.4 / Chapter 1.2.1 --- Definition --- p.4 / Chapter 1.2.2 --- Consequences of insomnia --- p.6 / Chapter 1.2.3 --- Prevalence --- p.8 / Chapter 1.2.4 --- Subtypes of insomnia --- p.9 / Chapter 1.2.5 --- Causes --- p.12 / Chapter 1.2.6 --- Treatment of insomnia --- p.13 / Chapter 1.2.6.1 --- Cognitive-behavioral therapy for insomnia --- p.14 / Chapter 1.2.6.2 --- Pharmacological treatment for insomnia --- p.17 / Chapter 1.3 --- Traditional Chinese medicine and herbs in SD formula --- p.22 / Chapter 1.4 --- Drosophila model for studying sleep --- p.25 / Chapter 1.4.1 --- Drosophila as a disease model --- p.25 / Chapter 1.4.2 --- Drosophila Sleep --- p.26 / Chapter 1.4.3 --- Similarity of Drosophila and mammalian sleep --- p.26 / Chapter 1.4.4 --- Methods for measuring Drosophila sleep --- p.29 / Chapter 1.4.4.1 --- Surrogate measurement of sleep in Drosophila --- p.31 / Chapter 1.5 --- Objectives of study --- p.33 / Chapter 2 --- Materials and Methods --- p.35 / Chapter 2.1 --- Preparation of the Sleep Disorder (SD) extract --- p.35 / Chapter 2.2 --- Establishment of the Drosophila sleep model --- p.38 / Chapter 2.2.1 --- Drosophila culture --- p.38 / Chapter 2.2.1.1 --- Fly stock --- p.38 / Chapter 2.2.1.2 --- Fly food --- p.38 / Chapter 2.2.1.3 --- Culture environment --- p.38 / Chapter 2.2.2 --- Preparation of flies for experiments --- p.39 / Chapter 2.2.3 --- Agar food and drug preparation --- p.39 / Chapter 2.2.4 --- Measurement of activity and sleep in fly --- p.40 / Chapter 2.2.5 --- Determining the effects of SD extract on Drosophila sleep --- p.40 / Chapter 2.2.5.1 --- Data analysis --- p.41 / Chapter 2.2.6 --- Test of amount of food intake for different dosages of SD using food dye --- p.41 / Chapter 2.2.7 --- Survival test --- p.42 / Chapter 2.3 --- Establishment of the Drosophila caffeine-induced insomnia model --- p.43 / Chapter 2.3.1 --- Determining the effects of caffeine on the Drosophila sleep --- p.43 / Chapter 2.3.2 --- Determining the effects of SD extract on the Drosophila caffeine-induced insomnia model --- p.43 / Chapter 2.3.2.1 --- HPLC determination of caffeine intake in Drosophila --- p.44 / Chapter 2.3.2.2 --- "Spectrophotometric measurement of caffeine, SD and caffeine-SD solutions" --- p.45 / Chapter 2.4 --- "Expression of Cyp6a8, Djun and Dfos in drug-treated Drosophila heads" --- p.46 / Chapter 2.4.1 --- Drug treatment and collection of fly head samples --- p.46 / Chapter 2.4.2 --- Total RNA extraction from fly heads --- p.46 / Chapter 2.4.3 --- Real-time polymerase chain reaction analysis --- p.48 / Chapter 2.5 --- Determining the effects of SD formula on short-sleep mutants --- p.51 / Chapter 2.5.1 --- Fly stocks --- p.51 / Chapter 2.5.2 --- Experimental design --- p.51 / Chapter 3. --- Results --- p.53 / Chapter 3.1 --- Establishment of the Drosophila sleep model --- p.53 / Chapter 3.1.1 --- Baseline activity and sleep --- p.53 / Chapter 3.1.2 --- Effect of SD on Drosophila sleep --- p.55 / Chapter 3.1.3 --- Amount of food intake for different dosages of SD --- p.57 / Chapter 3.1.4 --- Effect of SD on the survival of wide-type (CSI) flies --- p.59 / Chapter 3.2 --- Establishment of the caffeine-induced insomnia model in Drosophila --- p.61 / Chapter 3.2.1 --- Effect of Caffeine on Drosophila sleep --- p.61 / Chapter 3.2.2 --- Effect of the SD on the caffeine-induced wakefulness --- p.64 / Chapter 3.2.3 --- Validation of caffeine intake by HPLC --- p.68 / Chapter 3.2.4 --- "Spectra of caffeine, SD and caffeine-SD solutions" --- p.72 / Chapter 3.3 --- Effect of SD on the sleep of short-sleep mutants --- p.74 / Chapter 3.3.1 --- fumin mutant --- p.74 / Chapter 3.3.2 --- minisleep mutant --- p.78 / Chapter 3.3.3 --- HkY fly --- p.82 / Chapter 3.4 --- Effect of the SD and caffeine on gene expression --- p.86 / Chapter 3.4.1 --- Effect of the SD and caffeine on Cyp6a8 mRNA expression --- p.86 / Chapter 3.4.2 --- Effect of the SD and caffeine on Djun mRNA expression --- p.89 / Chapter 3.4.3 --- Effect of the SD and caffeine on Dfos mRNA expression --- p.91 / Chapter 4. --- Discussion --- p.93 / Chapter 4.1 --- Rationales for evaluating the effect of SD formula in Drosophila model --- p.94 / Chapter 4.2 --- Establishment of the Drosophila Sleep model --- p.96 / Chapter 4.2.1 --- Hypnotic effect of SD in Drosophila --- p.97 / Chapter 4.2.2 --- Toxicity of SD extract in fly --- p.98 / Chapter 4.3 --- Effect of SD on Drosophila caffeine-induced insomnia model --- p.100 / Chapter 4.3.1 --- Drug administration in Drosophila --- p.102 / Chapter 4.4 --- Effect of SD on Short-sleep mutant --- p.105 / Chapter 4.5 --- Study of gene expression by SD --- p.108 / Chapter 4.6 --- Limitations of the model --- p.112 / Chapter 5. --- Conclusion and Future Prospects --- p.115 / Chapter 5.1 --- Conclusion --- p.115 / Chapter 5.2 --- Future prospects --- p.115 / References --- p.117

Wong, Wai Yin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 92-108). / Abstracts in English and Chinese. / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Atherosclerosis --- p.1 / Chapter 1.1.1 --- Pathogenesis of Atherosclerosis --- p.2 / Chapter 1.1.2 --- Atherosclerosis and Cardiovascular Disease --- p.4 / Chapter 1.2 --- Cardiovascular Disease (CVD) --- p.5 / Chapter 1.2.1 --- Term Definition --- p.5 / Chapter 1.2.2 --- Risk Factors --- p.6 / Chapter 1.2.3 --- Current Western Medications --- p.7 / Chapter 1.3 --- Reactive Oxygen Species (ROS) --- p.8 / Chapter 1.3.1 --- Impact of ROS --- p.8 / Chapter 1.3.2 --- "Superoxide Anion Radical, Hydrogen Peroxide, Hydroxyl Radical, Nitric Oxide" --- p.9 / Chapter 1.3.3 --- ROS Production by NAD(P)H Oxidases --- p.11 / Chapter 1.3.4 --- ROS Production by Mitochondria --- p.12 / Chapter 1.3.5 --- Lipid Peroxidation --- p.13 / Chapter 1.3.6 --- Other Sources of ROS --- p.15 / Chapter 1.4 --- Antioxidants --- p.16 / Chapter 1.4.1 --- Superoxide Dismutase (SOD) --- p.16 / Chapter 1.4.2 --- Catalase (CAT) --- p.17 / Chapter 1.4.3 --- Glutathinoe Peroxidase (GPx) --- p.17 / Chapter 1.4.4 --- Glutathione-S-Transferase (GST) --- p.18 / Chapter 1.4.5 --- Vitamin E --- p.18 / Chapter 1.4.6 --- Vitamin C --- p.19 / Chapter 1.5 --- Ageing --- p.19 / Chapter 1.6 --- Antioxidants and CVD --- p.21 / Chapter 1.7 --- Traditional Chinese Medicine (TCM) --- p.22 / Chapter 1.7.1 --- Danshen --- p.23 / Chapter 1.7.2 --- Gegen --- p.25 / Chapter 1.7.3 --- Danshen-Gegen Compound Formula (DG) --- p.26 / Chapter 1.8 --- Aim of Study --- p.27 / Chapter Chapter 2 --- In vitro Foam Cells Formation --- p.29 / Chapter 2.1 --- Materials and Methods --- p.29 / Chapter 2.1.1 --- Materials --- p.29 / Chapter 2.1.2 --- Methods --- p.30 / Chapter 2.1.2.1 --- Herbal Preparation by Hot Water Extraction --- p.30 / Chapter 2.1.2.2 --- Resident Peritoneal Macrophages Preparation --- p.31 / Chapter 2.1.2.3 --- "Colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl Tetrazolium Bromide (MTT) Assay" --- p.31 / Chapter 2.1.2.4 --- DG Effect on in vitro Foam Cells Formation --- p.32 / Chapter 2.2 --- Results and Discussion --- p.32 / Chapter 2.3 --- Summary --- p.39 / Chapter Chapter 3 --- In vivo Antioxidant Level --- p.40 / Chapter 3.1 --- DG Effect on in vivo Antioxidant Levels on Young-adult Wistar Rats --- p.40 / Chapter 3.1.1 --- Materials and Methods --- p.40 / Chapter 3.1.1.1 --- Herbal Preparation by Hot Water Extraction --- p.40 / Chapter 3.1.1.2 --- Assay Kits --- p.41 / Chapter 3.1.1.3 --- Antibodies for Protein Expression Determination in Organs --- p.41 / Chapter 3.1.1.4 --- Animals and Experimental Design --- p.41 / Chapter 3.1.1.5 --- Plasma Antioxidants --- p.42 / Chapter 3.1.1.6 --- Lipid Peroxidation and Protein Expression in Organs --- p.46 / Chapter 3.1.1.7 --- Statistics --- p.52 / Chapter 3.1.2 --- Results and Discussion --- p.53 / Chapter 3.2 --- DG Effect on in vivo Antioxidant Levels on Middle-aged Wistar Rats --- p.74 / Chapter 3.2.1 --- Materials and Methods --- p.75 / Chapter 3.2.2 --- Results and Discussion --- p.75 / Chapter 3.3 --- Summary --- p.87 / Chapter Chapter 4 --- Conclusion and Future Work --- p.90 / Chapter 4.1 --- Conclusion --- p.90 / Chapter 4.2 --- Future work --- p.90 / Reference --- p.92 / Related Publication --- p.109

Estima-se que 170 milhões de pessoas no mundo estejam infectadas com o vírus da hepatite C (VHC), o que está altamente relacionado à ocorrência de hepatite crônica e carcinoma hepatocelular. A prevalência de esteatose hepática em doentes com hepatite C crônica é muito maior do que na população geral variando entre 40 a 75%. A associação entre a infecção pelo VHC e esteatose hepática é multifatorial. Duas formas de esteatose hepática são encontradas em pacientes com hepatite C crônica: esteatose metabólica (fatores de risco) e citopática relacionada ao genótipo 3a. Os lipídios são essenciais para o ciclo de replicação do VHC, eles podem exercer seu efeito em diferentes níveis como: grupos prostéticos em proteínas virais e/ou cofatores celulares na replicação de VHC, componentes especializados na estrutura do VHC onde ocorre a replicação ou como constituinte das partículas lipovirais. Trabalhos experimentais realizados anteriormente por nosso grupo relataram que a administração do composto natural Yo Jyo Hen Shi Ko (YHK) promove a inibição do desenvolvimento da esteatose, redução dos marcadores de estresse oxidativo, menor escore de inflamação, melhora nas concentrações de aminotransferases e diminuição da gordura visceral em um modelo animal de esteato-hepatite não alcoólica. A terapia padrão da hepatite C consiste em uma combinação de interferon peguilado alfa (PEG-IFN-alfa) que estimula o sistema imunológico do hospedeiro para combater a infecção e o composto antiviral ribavirina. Atualmente foram aprovados pelas agências de saúde os inibidores de protease Boceprevir, Telaprevir, Daclatasvir e Simeprevir. No entanto, sua eficiência varia entre os genótipos e as constantes mutações do vírus podem levar a resistência. A falta de uma vacina ou uma terapia definitiva faz com que diversos compostos com diferentes mecanismos de ação sejam testados como possíveis alternativas de tratamento. Tendo em vista a capacidade do YHK de reduzir a esteatose e a importância do metabolismo para a replicação do VHC, o objetivo deste trabalho foi avaliar o efeito do YHK no ciclo celular do VHC. Para isso foram utilizadas técnicas de cultura celular que permitem o estudo das diferenças fases do ciclo de replicação do VHC: entrada (VHCpp), replicação - replicons JFH1-NS3-5B e Con1, replicação e infecção- JC1-Fluc. De forma a elucidar a possibilidade de um único componente da fórmula YHK apresentar efeito sobre o VHC, foram utilizadas para comparação as substâncias ativas de seus ingredientes isoladamente: Panax pseudo ginseng - Notoginsenoside R1; Eucommia ulmoides -(±) Pinoresinol; Licorice root - Ácido Glicirrizínico. Os compostos não apresentaram efeitos na entrada, replicação e liberação de novas partículas virais. Devido à ausência de resultados bem delineados e tendo em vista os resultados das terapias anti-VHC atuais e futuras, é improvável que compostos naturais sejam utilizados ou chegarão ao desenvolvimento clínico nesta indicação / Worldwide is estimated that nearly 170 million people are infected with hepatitis C virus (HCV), highly correlated with the occurrence of chronic hepatitis and hepatocellular carcinoma. Hepatitis C patients present higher prevalence of steatosis when compared with the general population, ranging between 40% and 75%. There are two forms of steatosis in HCV infected patients: metabolic steatosis (risk factors) and cytopathic associated with genotype 3. Lipids are essential for the HCV replication cycle. It acts on different functions: as prosthetic groups into viral proteins and / or cellular cofactors in the HCV replication, as specific HCV components or as a constituent of lipovirals particles. Our group previously reported that the administration of the natural compound Yo Jyo Hen Shi Ko (YHK) inhibits steatosis development, decreases markers of oxidative stress and inflammation, improves aminotransferases concentration and decreases the visceral fat. Standard therapy for hepatitis C is a combination of pegylated interferon alpha (PEG-IFN-alfa), stimulating the host immune system to fight infection and the antiviral compound named ribavirin. Nowadays, Telaprevir, Boceprevir, Sofosbovir and Simeprevir are approved as new anti-HCV drugs; they act as protease inhibitors. Its efficiency, however, varies between genotypes, and the constant mutations of the virus can lead to resistance. The lack of vaccines, or a definitive therapy, stimulates the research of new compounds and alternative treatments. In this study, we evaluated the effect of YHK in HCV replication cycle due to the effect of YHK and the importance of lipid metabolism for HCV. For this purpose we used cell culture techniques allowing the study of different stages of HCV replication cycle: entry (HCVpp), replication - replicons JFH1 NS3-5B and Con1, also replication and infection-JC1-Fluc. We also used active compounds of its ingredients: Panax pseudo ginseng - Notoginsenoside R1; eucommia - (±) pinoresinol, Licorice root - Glycyrrhizinic Acid in order to elucidate a possible effect of a single component of the YHK formula in HCV. We could not observe any difference in HCV entry, replication and release in the presence of the four compounds. It is unlikely that natural compounds will be used or come to clinical development in this indication, due to the absence of well defined results and in view of the results of new anti-HCV therapies

Hoi, Chu Peng. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 81-103). / Abstracts in English and Chinese. / Acknowledgements --- p.II / Abstract --- p.III / Abstract (in Chinese) --- p.V / List of Abbreviations --- p.VI / List of Figures --- p.VIII / List of Tables --- p.X / Table of Contents --- p.XI / Chapter Chapter One --- General introduction --- p.1 / Chapter 1.1 --- Alzheimer's disease --- p.1 / Chapter 1.1.1 --- Epidemiology and risk factors --- p.2 / Chapter 1.1.2 --- Clinical manifestation and course --- p.4 / Chapter 1.1.3 --- Clinical diagnosis --- p.5 / Chapter 1.1.4 --- Neuropathology and pathogenesis of AD --- p.8 / Chapter 1.1.5 --- Drug therapy of AD --- p.11 / Chapter 1.1.5.1 --- Drugs for symptomatic treatment --- p.11 / Chapter 1.1.5.2 --- Drugs based on epidemiology --- p.12 / Chapter 1.1.5.3 --- Drugs with potential disease-modifying effects --- p.14 / Chapter 1.1.5.4 --- Herbal supplements --- p.15 / Chapter 1.2 --- Models for drug discovery in Alzheimer Disease --- p.15 / Chapter 1.2.1 --- In vivo (animal) models --- p.16 / Chapter 1.2.2 --- In vitro (cellular) models --- p.18 / Chapter 1.3 --- Chinese herbs for the treatment of AD --- p.20 / Chapter 1.3.1 --- Ginkgo biloba L --- p.21 / Chapter 1.3.2 --- Magnolia officinalis --- p.24 / Chapter 1.3.3 --- Acori graminei Rhizoma (AGR) --- p.26 / Chapter 1.3.4 --- Gastrodia elata (G. elata) --- p.27 / Chapter 1.3.5 --- Rhodiola rosea L.( R. rosea) --- p.29 / Chapter 1.3.6 --- Scutellariae baicalensis --- p.30 / Chapter 1.3.7 --- Curcuma longa L.(Zingiberaceae) --- p.31 / Chapter 1.4 --- Aims of the study --- p.33 / Chapter Chapter Two --- Materials and Methods --- p.34 / Chapter 2.1 --- Materials --- p.34 / Chapter 2.1.1 --- Chemicals and reagents --- p.34 / Chapter 2.1.2 --- Materials for cell culture --- p.35 / Chapter 2.1.3 --- Instruments --- p.35 / Chapter 2.2 --- Methods --- p.36 / Chapter 2.2.1 --- Cell culture --- p.36 / Chapter 2.2.2 --- MTT cell viability assay --- p.38 / Chapter 2.2.3 --- Characterization of the cytotoxicity of Aβ peptide in NGF-differentiated PC 12 cells --- p.38 / Chapter 2.2.4 --- Screening of the neuroprotective effect of major principles from selected herbs on PC 12 cells against Aβ-induced cytotoxicity --- p.39 / Chapter 2.2.5 --- Measurement of reactive oxygen species (ROS) --- p.40 / Chapter 2.2.6 --- Measurement of intracellular calcium levels --- p.41 / Chapter 2.2.7 --- Measurement of caspase-3 activity --- p.42 / Chapter 2.2.8 --- Propidium iodide (PI) staining to evaluate apoptosis and necrosis --- p.43 / Chapter 2.3 --- Statistics --- p.45 / Chapter Chapter Three --- Results --- p.46 / Chapter 3.1 --- NGF-differentiated PC 12 cells --- p.46 / Chapter 3.1.1 --- Determination of an appropriate cell density for the screening experiments --- p.46 / Chapter 3.1.2 --- Characterization of Aβ-induced cytotoxicity in NGF-differentiated PC 12 cells --- p.47 / Chapter 3.1.2.1 --- Cytotoxicity of Aβ-related fragments in NGF-differentiated PC 12 cells --- p.48 / Chapter 3.1.2.2 --- Dose-dependent cytotoxic effect of Aβ on PC 12 cells --- p.48 / Chapter 3.1.2.3 --- Time-dependent effect of Aβ-induced toxicity on PC12 cells --- p.50 / Chapter 3.1.3 --- Protective effect of selected active principles against Aβ1-4-induced toxicity in PC 12 cells --- p.51 / Chapter 3.2 --- Measurement of reactive oxygen species (ROS) --- p.54 / Chapter 3.2.1 --- Measurement of ROS induced by H202 --- p.54 / Chapter 3.2.2 --- Measurement of ROS induced by Aβ --- p.56 / Chapter 3.3 --- Measurement of Intracellular calcium levels --- p.57 / Chapter 3.4 --- Measurement of caspase-3 activity --- p.58 / Chapter 3.4.1 --- AMC reference standard curve --- p.59 / Chapter 3.4.2 --- Measurement of caspase-3 activity --- p.59 / Chapter 3.5 --- PI staining for evaluate apoptosis and necrosis --- p.60 / Chapter Chapter Four --- Discussion --- p.64 / Chapter 4.1 --- Aβ-induced cytotoxicity in NGF-differentiated PC 12 cells as an in vitro model of Alzheimer's disease --- p.64 / Chapter 4.1.1 --- Cell line selection --- p.65 / Chapter 4.1.2 --- Characterization of Aβ-induced cytotoxicity in NGF-differentiated PC 12 cells --- p.66 / Chapter 4.2 --- Screening of the neuroprotective effects of selected active principles against Aβ-induced cytotoxicity in NGF-differentiated PC 12 cells --- p.67 / Chapter 4.3 --- Neuroprotection via inhibition of the ROS generation --- p.71 / Chapter 4.4 --- Neuroprotection via suppression of calcium homeostasis --- p.73 / Chapter 4.5 --- Neuroprotective via inhibition of Aβ-induced apoptosis --- p.75 / Chapter 4.5.1 --- Inhibition of caspase-3 activation --- p.75 / Chapter 4.5.2 --- PI staining for evaluation of apoptosis and necrosis --- p.76 / Chapter Chapter Five --- Conclusion and future work --- p.79 / Chapter 5.1 --- Conclusion --- p.79 / Chapter 5.2 --- Future work --- p.80 / References --- p.81

Lam Rosanna Yen Yen. / Thesis submitted in: September 2004. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (leaves 142-154). / Abstracts in English and Chinese. / Abstract --- p.i / Chinese Abstract --- p.iii / Acknowledgements --- p.v / Table of Contents --- p.vi / List of Abbreviations --- p.xii / List of Figures --- p.xv / List of Tables --- p.xix / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Reactive oxygen species --- p.1 / Chapter 1.1.1 --- Intracellular sources of ROS --- p.1 / Chapter 1.1.2 --- Extracellular sources of ROS --- p.2 / Chapter 1.1.3 --- Superoxide anion radicals --- p.2 / Chapter 1.1.4 --- Hydrogen peroxide --- p.3 / Chapter 1.1.5 --- Hydroxyl radicals --- p.3 / Chapter 1.1.6 --- Singlet oxygen --- p.4 / Chapter 1.1.7 --- Peroxyl radicals and peroxides --- p.4 / Chapter 1.1.8 --- Damage of cellular structures by ROS --- p.5 / Chapter 1.2 --- Antioxidative defence in the body --- p.6 / Chapter 1.2.1 --- Antioxidant proteins --- p.6 / Chapter 1.2.2 --- Antioxidant enzymes --- p.6 / Chapter 1.2.3 --- Antioxidant compounds --- p.7 / Chapter 1.2.3.1 --- Vitamin E --- p.8 / Chapter 1.2.3.2 --- Vitamin C --- p.9 / Chapter 1.2.3.3 --- Glutathione --- p.9 / Chapter 1.2.3.4 --- Urate --- p.9 / Chapter 1.2.3.4.1 --- Purine metabolism --- p.10 / Chapter 1.2.3.4.2 --- Xanthine oxidase --- p.12 / Chapter 1.2.4 --- Oxidative stress and antioxidant defence mechanisms in RBC --- p.12 / Chapter 1.2.5 --- Oxidative stress and antioxidant defence mechanisms in LDL --- p.16 / Chapter 1.3 --- Human diseases originated from pro-oxidant conditions --- p.16 / Chapter 1.3.1 --- Atherosclerosis --- p.17 / Chapter 1.3.2 --- Ischemia /reperfusion injury --- p.17 / Chapter 1.3.3 --- Glucose-6-phosphate dehydrogenase deficiency --- p.18 / Chapter 1.3.4 --- DNA mutation --- p.18 / Chapter 1.3.5 --- Other pro-oxidant state related diseases --- p.19 / Chapter 1.4 --- Hyperuricemia and gout: diseases originated from an extreme antioxidant condition --- p.19 / Chapter 1.4.1 --- Inhibition of XOD as a treatment method for hyperuricemia --- p.20 / Chapter 1.4.2 --- Relationship between ROS injury and hyperuricemia --- p.22 / Chapter 1.5 --- Antioxidants in human nutrition --- p.23 / Chapter 1.6 --- Chinese medicinal therapeutics --- p.23 / Chapter 1.6.1 --- Rhubarb --- p.25 / Chapter 1.6.2 --- Aloe --- p.26 / Chapter 1.6.3 --- Ginger --- p.27 / Chapter 1.6.4 --- Objectives of the project --- p.30 / Chapter 1.6.5 --- Strategies applied to achieve the objectives of the present project --- p.30 / Chapter Chapter 2 --- Materials and methods --- p.31 / Chapter 2.1 --- XOD inhibition assay --- p.31 / Chapter 2.1.1 --- Assay development --- p.31 / Chapter 2.1.2 --- Dose-dependent study --- p.32 / Chapter 2.1.3 --- Reversibility of the enzyme inhibition --- p.32 / Chapter 2.1.4 --- Lineweaver-Burk plots --- p.33 / Chapter 2.2 --- Lipid peroxidation inhibition assay of mouse liver microsomes --- p.34 / Chapter 2.2.1 --- Preparation of mouse liver microsomes --- p.34 / Chapter 2.2.2 --- Basis of assay --- p.34 / Chapter 2.2.3 --- Assay procedures --- p.35 / Chapter 2.3 --- AAPH-induced hemolysis inhibition assay --- p.36 / Chapter 2.3.1 --- Preparation of RBC --- p.36 / Chapter 2.3.2 --- Basis of assay --- p.36 / Chapter 2.3.3 --- Assay procedures --- p.37 / Chapter 2.4 --- Lipid peroxidation inhibition assay of RBC membrane --- p.38 / Chapter 2.4.1 --- Preparation of RBC membrane --- p.38 / Chapter 2.4.2 --- Basis of assay --- p.39 / Chapter 2.4.3 --- Assay procedures --- p.40 / Chapter 2.5 --- ATPase protection assay --- p.41 / Chapter 2.5.1 --- Preparation of RBC membrane --- p.41 / Chapter 2.5.2 --- Preparation of malachite green (MG) reagent --- p.41 / Chapter 2.5.3 --- Basis of assay --- p.41 / Chapter 2.5.4 --- Assay procedures --- p.42 / Chapter 2.5.5 --- Determination of ATPase activities --- p.43 / Chapter 2.5.6 --- Assay buffers --- p.43 / Chapter 2.6 --- Sulfhydryl group protection assay --- p.44 / Chapter 2.6.1 --- Preparation of RBC membrane --- p.44 / Chapter 2.6.2 --- Basis of assay --- p.45 / Chapter 2.6.3 --- Assay procedures --- p.45 / Chapter 2.7 --- Lipid peroxidation inhibition assay of LDL by the AAPH method --- p.46 / Chapter 2.7.1 --- Basis of assay --- p.46 / Chapter 2.7.2 --- Assay procedures --- p.46 / Chapter 2.8 --- Lipid peroxidation inhibition assay of LDL by the hemin method --- p.47 / Chapter 2.8.1 --- Basis of assay --- p.47 / Chapter 2.8.2 --- Assay procedures --- p.47 / Chapter 2.9 --- Protein assay --- p.48 / Chapter 2.10 --- Statistical analysis --- p.48 / Chapter 2.11 --- Test compounds --- p.48 / Chapter Chapter 3 --- Xanthine oxidase inhibition assay: results and discussion --- p.49 / Chapter 3.1 --- Introduction --- p.49 / Chapter 3.2 --- Results --- p.54 / Chapter 3.3 --- Discussion --- p.59 / Chapter Chapter 4 --- Lipid peroxidation inhibition in mouse liver microsomes: results and discussion --- p.64 / Chapter 4.1 --- Introduction --- p.64 / Chapter 4.2 --- Results --- p.64 / Chapter 4.3 --- Discussion --- p.69 / Chapter Chapter 5 --- Assays on protection of RBC from oxidative damage: results and discussion --- p.71 / Chapter 5.1 --- Introduction --- p.71 / Chapter 5.2 --- Results --- p.75 / Chapter 5.2.1 --- AAPH-induced hemolysis inhibition assay --- p.75 / Chapter 5.2.2 --- Lipid peroxidation inhibition assay of RBC membranes --- p.82 / Chapter 5.2.3 --- Ca2+-ATPase protection assay --- p.88 / Chapter 5.2.4 --- Na+/K+-ATPase protection assay --- p.95 / Chapter 5.2.5 --- Sulfhydryl group protection assay --- p.100 / Chapter 5.3 --- Discussion --- p.110 / Chapter 5.3.1 --- AAPH-induced hemolysis inhibition assay --- p.110 / Chapter 5.3.2 --- Lipid peroxidation inhibition assay of RBC membranes --- p.111 / Chapter 5.3.3 --- Ca2+-ATPase protection assay --- p.113 / Chapter 5.3.4 --- Na+/K+-ATPase protection assay --- p.114 / Chapter 5.3.5 --- Sulfhydryl group protection assay --- p.115 / Chapter 5.3.6 --- Chapter summary --- p.117 / Chapter Chapter 6 --- Lipid peroxidation inhibition assay of LDL: results and discussion --- p.118 / Chapter 6.1 --- Introduction --- p.118 / Chapter 6.2 --- Results --- p.118 / Chapter 6.3 --- Discussion --- p.134 / Chapter Chapter 7 --- General discussion --- p.137 / References --- p.142

Tang Sze-Wan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (leaves 104-118). / Abstracts in English and Chinese. / Abstract --- p.i / Abstract (Chinese) --- p.iii / Acknownledgement --- p.iv / List of Abbreviations --- p.v / List of Tables --- p.vii / List of Figures --- p.viii / Table of Contents --- p.xi / Chapter Chapter 1 - --- Introduction / Chapter 1.1 --- Trichosanthes spp --- p.1 / Chapter 1.1.1 --- Use of Trichosanthes --- p.2 / Chapter 1.1.2 --- Trichosanthin --- p.2 / Chapter 1.1.3 --- Karasurin --- p.5 / Chapter 1.1.4 --- Ribosome Inactivating Proteins --- p.6 / Chapter 1.1.5 --- Immunosuppresion --- p.7 / Chapter 1.1.6 --- Anti-Cancer Activity --- p.8 / Chapter 1.1.7 --- Miscellaneous Uses --- p.8 / Chapter 1.2 --- Cancer --- p.9 / Chapter 1.2.1 --- Oncogenes --- p.10 / Chapter 1.2.2 --- Tumor-Suppressor Genes --- p.11 / Chapter 1.2.3 --- Stability Genes --- p.12 / Chapter 1.2.4 --- Types of Cancer --- p.13 / Chapter 1.2.5 --- Cancer Therapy --- p.13 / Chapter 1.2.6 --- Apoptosis --- p.14 / Chapter 1.3 --- Chronic Myelogenous Leukemia (CML) --- p.17 / Chapter 1.3.1 --- Philadelphia Chromosome and BCR-ABL gene --- p.18 / Chapter 1.3.2 --- Treatment of CML --- p.20 / Chapter 1.4 --- Dendritic Differentiation of LC976 on K-562 --- p.20 / Chapter 1.4.1 --- Dendritic Cells --- p.21 / Chapter 1.4.2 --- Cancer Vaccine Development of Leukemia --- p.22 / Chapter 1.4.3 --- Dendritic differentiation of K-562 cells --- p.23 / Chapter 1.5 --- Perspective of the Project --- p.23 / Chapter Chapter 2 - --- Materials and Methods / Chapter 2.1 --- Materials / Chapter 2.1.1 --- Chemicals and Reagents --- p.25 / Chapter 2.1.2 --- Bioassay Kits --- p.26 / Chapter 2.1.3 --- Human Cell Lines --- p.26 / Chapter 2.1.4 --- Lab Wares and Equipments --- p.28 / Chapter 2.2 --- Extraction of LC9 --- p.76 / Chapter 2.2.1 --- Chemical Properties of the Lead Compound --- p.28 / Chapter 2.2.2 --- Crude Extraction of Trichosanthes sp --- p.29 / Chapter 2.2.3 --- Purification by Reversed-Phase Column --- p.29 / Chapter 2.2.4 --- Lyophilization and Preparation of LC976 --- p.31 / Chapter 2.3 --- Anti-Proliferation Effect of LC976 on Human Cell Lines / Chapter 2.3.1 --- Maintenance of Cell Lines --- p.32 / Chapter 2.3.2 --- MTT Assay --- p.32 / Chapter 2.3.3 --- BrdU Cell Proliferation ELISA --- p.34 / Chapter 2.4 --- Apoptosis Induction on K-5 --- p.62 / Chapter 2.4.1 --- PI Staining --- p.35 / Chapter 2.4.2 --- Annexin V-FITC FACS Analysis --- p.36 / Chapter 2.4.3 --- Caspase Activation --- p.37 / Chapter 2.5 --- Effect on Normal Human Lymphocytes / Chapter 2.5.1 --- Preparation of Human Normal Lymphocytes --- p.38 / Chapter 2.5.2 --- MTT Cell Viability Assay --- p.38 / Chapter 2.5.3 --- PI Staining --- p.39 / Chapter 2.5.4 --- Annexin V-FITC FACS Analysis --- p.39 / Chapter Chapter 3 - --- Results / Chapter 3.1 --- Extraction of LC976 --- p.40 / Chapter 3.2 --- LC976 Inhibited Proliferation of Human Cell Lines / Chapter 3.2.1 --- MTT Assay --- p.41 / Chapter 3.2.2 --- BrdU Cell Proliferation ELISA --- p.52 / Chapter 3.3 --- LC976 Induced Apoptosis in K-562 Cells / Chapter 3.3.1 --- PI Staining --- p.63 / Chapter 3.3.2 --- Annexin V-FITC FACS Analysis --- p.70 / Chapter 3.3.3 --- Caspase Activation --- p.73 / Chapter 3.4 --- Effect on Normal Human Lymphocytes / Chapter 3.4.1 --- MTT Cell Viability Assay --- p.76 / Chapter 3.4.2 --- PI Staining --- p.78 / Chapter 3.4.3 --- Annexin V-FITC FACS Analysis --- p.82 / Chapter Chapter 4 - --- Discussion / Chapter 4.1 --- Extraction of LC976 --- p.85 / Chapter 4.2 --- LC976 Inhibited Proliferation of Human Cell Lines / Chapter 4.2.1 --- MTT Assay --- p.86 / Chapter 4.2.2 --- BrdU Cell Proliferation ELISA --- p.88 / Chapter 4.3 --- LC976 induced Apoptosis in K-562 Cells / Chapter 4.3.1 --- PI Staining --- p.90 / Chapter 4.3.2 --- Annexin V-FITC Analysis --- p.95 / Chapter 4.3.3 --- Caspase Activation --- p.96 / Chapter 4.4 --- Effect on Normal Human Lymphocytes / Chapter 4.4.1 --- MTT Cell Viability Assay --- p.98 / Chapter 4.4.2 --- PI Staining --- p.99 / Chapter 4.4.3 --- Annexin V-FITC FACS Analysis --- p.100 / Chapter 4.5 --- Conclusion --- p.103 / Reference --- p.104

Yu, Wai Lam. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 79-88). / Abstracts in English and Chinese. / Acknowledgements --- p.IV / Abstract --- p.V / 論文摘要 --- p.VII / Table of Contents --- p.IX / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Cancer --- p.1 / Chapter 1.2 --- Hepatocellular Carcinoma (HCC) --- p.2 / Chapter 1.2.1 --- Risk factors causing HCC --- p.3 / Chapter 1.2.2 --- Molecular mechanism of HCC --- p.7 / Chapter 1.2.3 --- Treatment of HCC --- p.8 / Chapter 1.3 --- Tetrandrine (Tet) - A Natural Compound Derived from Traditional Chinese Medicine (TCM) --- p.10 / Chapter 1.3.1 --- Traditional Chinese Medicine (TCM) --- p.10 / Chapter 1.3.2 --- Tetrandrine (Tet) --- p.12 / Chapter 1.4 --- Molecular View of Apoptosis --- p.14 / Chapter 1.4.1 --- Overview of apoptosis --- p.14 / Chapter 1.4.2 --- Caspase cascade --- p.15 / Chapter 1.4.3 --- Bcl-2 protein family --- p.18 / Chapter 1.4.4 --- The role of mitochondria in apoptosis --- p.20 / Chapter 1.5 --- Anti-cancer Agents Inducing Apoptosis Are New Targets --- p.22 / Chapter 1.6 --- Aim of Study --- p.26 / Chapter Chapter 2 --- Materials and Methods --- p.27 / Chapter 2.1 --- Cell Culture And Treatment --- p.27 / Chapter 2.1.1 --- Cell lines used --- p.27 / Chapter 2.1.2 --- Tetrandrine (Tet) --- p.28 / Chapter 2.1.3 --- Chemicals and reagents 2 --- p.83 / Chapter 2.1.4 --- Solution preparation --- p.29 / Chapter 2.1.5 --- Procedures --- p.30 / Chapter 2.2 --- Cell viability --- p.32 / Chapter 2.2.1 --- Chemicals and reagents . --- p.32 / Chapter 2.2.2 --- Solution preparation --- p.32 / Chapter 2.2.3 --- Procedures --- p.32 / Chapter 2.3 --- Apoptosis detection --- p.34 / Chapter 2.3.1 --- Chemicals and reagents --- p.34 / Chapter 2.3.2 --- Solution preparation --- p.35 / Chapter 2.3.3 --- Procedures --- p.36 / Chapter 2.4 --- Gene expression in tet-induced apoptotic cells --- p.39 / Chapter 2.4.1 --- Chemicals and reagents --- p.39 / Chapter 2.4.2 --- Solution preparation --- p.40 / Chapter 2.4.3 --- Procedures --- p.40 / Chapter 2.5 --- Protein expression in tet-induced apoptotic cells --- p.44 / Chapter 2.5.1 --- Chemicals and reagents --- p.44 / Chapter 2.5.2 --- Solution preparation --- p.45 / Chapter 2.5.3 --- Procedures --- p.48 / Chapter 2.6 --- Cell cycle analysis of tet-treated cells --- p.54 / Chapter 2.5.1 --- Chemicals and reagents --- p.54 / Chapter 2.5.2 --- Solution preparation --- p.54 / Chapter 2.5.3 --- Procedures --- p.54 / Chapter Chapter 3 --- Result --- p.56 / Chapter Chapter 4 --- Discussion --- p.70 / Chapter 4.1 --- Dose- and Time- Dependent Inhibitory Effects of Tet were found on HuH-7 And JHH-4 Cell Lines --- p.70 / Chapter 4.2 --- Tet Is More Selective Towards Liver Cancer Cells --- p.71 / Chapter 4.3 --- The Cell Death in HuH-7 Cells Induced by Tet is Mediated Through Apoptosis --- p.72 / Chapter 4.4 --- Hepatocellular Carcinoma (HCC)Tet Induces G1 Phase Cell Cycle Arrest as Part of Its Mechanism in Inducing Apoptosis in HuH-7 Cells --- p.73 / Chapter 4.5 --- Tet Could Probably Induce G1 Phase Cell Cycle Arrest in JHH-4 Cells --- p.75 / Chapter 4.6 --- "Tet-induced Apoptosis Involves the Intrinsic, Caspase-Dependent Pathway in Both the HuH-7 and JHH-4 Cell Lines" --- p.75 / Chapter 4.7 --- Proteins in Bcl-2 Family are Involved in the Inhibitory Mechanism of Tet --- p.77 / Reference --- p.79

Hong, Sijia. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 197-234). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Woo Yiu Ho Anthony. / "August 2004." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (p. 176-198). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Eighty-two patients with breast cancer, twenty-seven patients with nasopharyngeal carcinoma and sixty-five patients with rheumatoid arthritis in this study were selected based on voluntary, randomization and double blind grouping criteria. / In nasopharyngeal carcinoma patients, the decrease in percentage and the absolute count of T lymphocytes in the TCM group was significantly lower than those in the placebo group. Besides, the decrease of the absolute count of T helper and T suppressor in the TCM group was significantly lower than that in the placebo group (all p < 0.05). The decrease may be due to radiotherapy. However, there was no significant difference in plasma sIL-2R and soluble tumor necrosis factor receptor 2 (sTNFR2) between the TCM group and the placebo group. / In rheumatoid arthritis patients, there was no significant difference in plasma. C-reactive protein (CRP), in the percentage, absolute count, and the ratio of CD4+/CD8+/NK/B lymphocytes between the TCM group and the placebo group. / Results showed that the absolute count of T helper lymphocytes (CD4+), the ratio of T helper lymphocytes (CD4+)/T suppressor and cytotoxic lymphocytes (CD8+), and the percentage and the absolute count of B lymphocytes were significantly elevated in the patients with breast cancer after taking Yunzhi-Danshen capsules, while plasma soluble interleukin-2 receptor (sIL-2R) concentration was significantly decreased (all p < 0.05). / This study shows that the selected traditional Chinese medicine have determinable immunomodulatory effects in patients with cancer and rheumatoid arthritis. (Abstract shortened by UMI.) / Traditional Chinese medicine (TCM) has been used to treat chronic diseases and tumor allegedly by immunomodulatory mechanisms. Breast cancer and nasopharyngeal cancer are prevalent carcinoma diseases in Hong Kong. The immune system of such patients could be adversely affected during the course of conventional chemotherapy or radiotherapy. Rheumatoid arthritis is an inflammatory autoimmune disease of the joints. The aim of this study was to assess the immunomodulatory effects of TCM Yunzhi-Danshen in auxiliary treatment of both kinds of cancer patients, and Lingzhi (Ganoderma Lucidum)-San Miao San ( Atractylodes lancea, Phellodendron amurense and Achyranthes bidentata B1) in supplementation treatment of patients with rheumatoid arthritis. / by Bao Yixi. / "July 2005." / Adviser: Wai-Kei Lam. / Source: Dissertation Abstracts International, Volume: 67-01, Section: B, page: 0166. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (p. 150-167). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese. / School code: 1307.