Chan Yin Ling. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (leaves 147-167). / Abstracts in English and Chinese. / ABSTRACT --- p.III / ACKNOWLEDGEMENT --- p.X / TABLE OF CONTENTS --- p.XI / ABBREVIATIONS --- p.XV / LIST OF FIGURES --- p.XVII / LIST OF TABLES --- p.XXI / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Introduction to Cardiovascular Disease and Atherosclerosis --- p.1 / Chapter 1.1.1 --- Cardiovascular Disease --- p.1 / Chapter 1.1.2 --- A therosclerosis --- p.3 / Chapter 1.1.2.1 --- Structure of Arteries --- p.4 / Chapter 1.1.2.2 --- Pathophysiology of Atherosclerosis --- p.5 / Chapter 1.1.2.3 --- Endothelial Dysfunction --- p.8 / Chapter 1.1.3 --- Current Western Therapies --- p.11 / Chapter 1.1.3.1 --- Surgery --- p.11 / Chapter 1.1.3.2 --- Western Medications --- p.13 / Chapter 1.1.4 --- Traditional Chinese Medicine --- p.17 / Chapter 1.1.4.1 --- Long History --- p.17 / Chapter 1.1.4.2 --- As Alternative Medicine --- p.18 / Chapter 1.1.4.3 --- Modernization of Chinese Medicine --- p.19 / Chapter 1.2 --- Introduction and Selection of Chinese Medicine --- p.20 / Chapter 1.2.1 --- Selection ofTCM Formulation from Pharmacopoeia --- p.20 / Chapter 1.2.1.1 --- Compound Formulation --- p.20 / Chapter 1.2.2 --- Introduction to the Herbal Medicines --- p.21 / Chapter 1.2.2.1 --- Danshen (Salvia miltiorrhiza) --- p.21 / Chapter 1.2.2.2 --- Gegen (Puerariae thomsonii and Puerariae lobata) --- p.22 / Chapter 1.2.2.3 --- Yanhu (Corydalis yanhusuo) and its Exclusion --- p.24 / Chapter 1.2.3 --- Source and Authentication of the Herbal Medicines --- p.25 / Chapter CHAPTER 2 --- OPTIMIZATION OF DANSHEN-GEGEN FORMULA --- p.26 / Chapter 2.1 --- Project History --- p.26 / Chapter 2.2 --- aims for the present study --- p.27 / Chapter 2.3 --- Methods and Materials --- p.30 / Chapter 2.3.1 --- Extracts --- p.30 / Chapter 2.3.2 --- Extraction Process --- p.31 / Chapter 2.3.3 --- In vitro Antioxidation Model --- p.33 / Chapter 2.3.4 --- Ex vivo Vasodilation Model --- p.35 / Chapter 2.3.5 --- Statistical Analysis --- p.38 / Chapter 2.4 --- Results --- p.39 / Chapter 2.4.1 --- Vasodilation Results --- p.39 / Chapter 2.4.2 --- Antioxidation Results --- p.43 / Chapter 2.5 --- Discussion --- p.46 / Chapter 2.6 --- Further Modification of the Formula --- p.49 / Chapter 2.6.1 --- Extracts --- p.49 / Chapter 2.6.2 --- Results --- p.49 / Chapter 2.7 --- discussion --- p.52 / Chapter CHAPTER 3 --- MARKER CHEMICAL CONTENTS OF HERBAL EXTRACTS AND THEIR PHARMACOLOGICAL PROPERTIES --- p.56 / Chapter 3.1 --- HPLC Analysis of Marker Contents --- p.56 / Chapter 3.1.1 --- Methods --- p.57 / Chapter 3.1.2 --- Results --- p.58 / Chapter 3.1.2.1 --- HPLC Chromatograms --- p.59 / Chapter 3.1.2.2 --- Content Percentage of Marker Compounds --- p.63 / Chapter 3.1.3 --- Discussion --- p.64 / Chapter 3.2 --- Studies on Marker Compounds --- p.65 / Chapter 3.2.1 --- Introduction --- p.65 / Chapter 3.2.2 --- Methods and Materials --- p.67 / Chapter 3.2.2.1 --- Source of Pure Compounds --- p.67 / Chapter 3.2.2.2 --- Purification and Identification of SAB --- p.68 / Chapter 3.2.2.3 --- Vasodilation model --- p.70 / Chapter 3.2.2.4 --- Antioxidation Model --- p.71 / Chapter 3.2.2.5 --- Structures of Pure Compounds --- p.72 / Chapter 3.2.3 --- Results --- p.73 / Chapter 3.2.3.1 --- Vasodilation Results --- p.73 / Chapter 3.2.3.2 --- Antioxidation Results --- p.76 / Chapter 3.3 --- Discussion --- p.79 / Chapter 3.4 --- Synergistic Effect Study --- p.85 / Chapter 3.4.1 --- Introduction --- p.85 / Chapter 3.4.2 --- Methods --- p.85 / Chapter 3.4.3 --- Results --- p.86 / Chapter 3.4.4 --- Discussion --- p.88 / Chapter 3.5 --- STUDY ON 3'-HYDROXYPlIERARIN AND 3'-METHOXYPUERARIN PURIFIED FROM YFGE --- p.90 / Chapter 3.5.1 --- 3 '-hydroxypuerarin and 3'-methoxypuerarin --- p.90 / Chapter 3.5.2 --- Methods and Materials --- p.91 / Chapter 3.5.2.1 --- Purification by HPLC semi-preparation --- p.91 / Chapter 3.5.2.2 --- Bioassays --- p.93 / Chapter 3.5.3 --- Results --- p.94 / Chapter 3.5.3.1 --- Vasodilation Study --- p.94 / Chapter 3.5.3.2 --- Antioxidative Effect of Yege --- p.95 / Chapter 3.5.4 --- Discussion / Chapter CHAPTER 4 --- MECHANISTIC STUDY --- p.98 / Chapter 4.1 --- Introduction --- p.98 / Chapter 4.1.1 --- Nitric Oxide-mediated Vasodilation --- p.99 / Chapter 4.1.2 --- Prostacyclin-mediated Vasodilation --- p.100 / Chapter 4.1.3 --- EDHF-mediated Vasodilation --- p.101 / Chapter 4.1.4 --- Endothelium-dependent and -independent Vasodilations --- p.103 / Chapter 4.2 --- Methods and Materials --- p.104 / Chapter 4.3 --- Results --- p.107 / Chapter 4.3.1 --- Danshen-Gegen Formula (DY80) --- p.107 / Chapter 4.3.2 --- Salvianolic acid B --- p.112 / Chapter 4.3.3 --- Daidzein --- p.117 / Chapter 4.4 --- Discussion --- p.121 / Chapter CHAPTER 5 --- STUDY ON LIPID PEROXIDATION AND UPTAKE BY MACROPHAGES --- p.128 / Chapter 5.1 --- Study of DY 80 and SAB on Copper-ion induced Low Density Lipoprotein Oxidation --- p.128 / Chapter 5.1.1 --- Pathologic Role of oxidized Low Density Lipoprotein --- p.128 / Chapter 5.1.2 --- Antioxidants in Low Density Lipoprotein and Role of Transition Metals --- p.129 / Chapter 5.1.3 --- Methods and Materials --- p.130 / Chapter 5.1.4 --- Results --- p.131 / Chapter 5.1.5 --- Discussion --- p.133 / Chapter 5.2 --- Study of Scavenger Receptor Regulation in Macrophages --- p.135 / Chapter 5.2.1 --- Introduction --- p.135 / Chapter 5.2.2 --- Methods and Materials --- p.136 / Chapter 5.2.3 --- Results --- p.139 / Chapter 5.2.4 --- Discussions --- p.140 / Chapter CHAPTER 6 --- General Discussion --- p.143 / REFERENCES --- p.147

Finally, the neuroprotective effects of TGP against corticosterone-induced neurotoxicity in rat pheochromocytoma (PC12) cells, an in vitro experimental model of depression were studied. The results showed TGP treatment dose-dependently protected the cells against corticosterone-induced toxicity. The cytoprotection afforded by TGP treatment was shown to be associated with an enhanced antioxidant activity, and increased expressions of neurotrophins including brain-derived neurotrophic factor, nerve growth factor and neurotrophin-3. / Secondly, the antidepressant-like effect of TGP was evaluated by a rat model of depression induced by chronic unpredictable mild stress (CUMS). The results showed that a 5-week CUMS caused depression-like behavior in rats, as indicated by a significant decreases in sucrose consumption (assessed by sucrose preference test) and locomotor activity (assessed by open-field test), and an increase in immobility time (assessed by forced swim test). Intragastric administration of TGP during the five weeks of CUMS procedure significantly suppressed these behavioral changes induced by CUMS. / Taken together, the results confirmed the antidepressant-like effect of TGP. The antidepressive action of TGP may be mediated by the modulation of the hypothalamic-pituitary-adrenal axis function, the inhibition of oxidative stress, and the up-regulation of neurotrophins, thereby leading to the neuroprotective effects. / The antidepressant-like effect of TGP was firstly evaluated by the behavioral despair test, forced swim test and tail suspension test. The results showed that intragastric administration of TGP caused a significant reduction of immobility time in both forced swim and tail suspension tests in mice. TGP treatment also significantly reduced the duration of immobility time in the forced swim test in rats. / The root of Paeonia lactiflora Pall. (Family: Ranunculaceae), commonly known as peony, is a component herb of many traditional formulae for the treatment of depression-like disorders. Previous studies have demonstrated the antidepressive effect of peony extract in mouse models of depression. Total glycosides of peony (TGP) is regarded as the major active ingredients of peony. The present study aims to confirm the antidepressive potential of TGP and evaluate its action mechanisms. / Thirdly, the neuroprotective effects of TGP on CUMS-treated rats and its possible mechanisms were investigated. The results showed that treatment with TGP for 5 weeks produced neuroprotective effects on the hippocampus of CUMS-treated rats. This effect was associated with the attenuation of hypothalamic-pituitary-adrenal axis hyperactivation (characterized by a decreased serum corticosterone level and an increased hippocampal glucocorticoid receptor expression), an inhibition of oxidative stress, and up-regulation of neurotrophins such as brain-derived neurotrophic factor and neurotrophin-3 in the hippocampus. / Mao, Qingqiu. / Adviser: Che Chun-Tao. / Source: Dissertation Abstracts International, Volume: 73-01, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 158-186). / 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, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Chung Hoi Sing. / "August 2001." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (p. 186-204) / 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.

Bioassays of total alkaloids of S. tuberosa samples representing the four types of chemical profiles were conducted on guinea pigs using citric acid aerosol for inducing cough. These results demonstrated their antitussive properties and thus suggested the possibility of other antitussive alkaloids than neotuberostemonine in S. tuberosa. So it became necessary to identify the major components in the samples of S. tuberosa representing the four types of chemical profiles. / Bioassays on guinea pigs of the four major components of S. tuberosa demonstrated their antitussive properties. Except a lower potency in tuberostemonine, antitussive effects of croomine and stemoninine showed similar or even stronger potency than neotuberostemonine at 25 and 50 mg/kg by intragastric administration. These four antitussive alkaloids could be used as lead compounds for the development of new antitussive drugs and as bioactive markers in quality control of the herb S. tuberosa and related products. / Cough is an airway defensive reflex, which is responsible for keeping the airway free of obstruction and harmful substances. As the commonest symptom for which medical advices is sought, enormous costs are spent on cough treatments. Regretfully, currently used antitussives are less than satisfactory due to their low potency or obvious side effects. So it is necessary to continue developing new and better antitussives. / Electrical stimulation of the superior laryngeal nerve on guinea pigs at 100 mg/kg through intraperitoneal administration indicated that croomine acted on the central pathway of cough reflex accompanied by respiratory depression. On the other hand, neotuberostemonine, tuberostemonine and stemoninine acted on the peripheral pathway without any observable side effects. These three alkaloids could be promising for developing new peripherally acting antitussives. Further, tuberostemonine was tested on primary cultured nodose ganglion cells by patch clamp and, at 0.5 mM, was demonstrated to significantly decrease the change amplitude of membrane potential induced by 1.0 mM citric acid solution. The results suggested that tuberostemonine could depress electrical excitability of nodose ganglion cells and thus inhibit the afferent signals of cough reflex leading to its antitussive activity. / In order to determine if the different chemical profiles of Stemona total alkaloids were the result of species difference or variations within the same species, the three Stemona species registered in the PRC Pharmacopoeia were collected from different areas in China. They were planted to flowering in our greenhouse and authenticated by both reproductive and vegetative characters. Microscopic examination on these authentic species showed that tuberous roots of S. tuberosa differed by epidermal cells with smooth outer surface and fibers in the cortex and pith from those of S. japonica and S. sessilifolia. The chemical profiles of authentic samples were analyzed on a HPLC-ELSD system. The results indicated that species-specific differences were present in the HPLC profiles of the three Stemona species. Within S. tuberosa, the chemical profiles of different samples were found to be very variable and they could be roughly divided into four types in the tested samples. Neotuberostemonine was present in one of the four types of S. tuberosa. Since antitussive effects of neotuberostemonine were demonstrated by Chung et al. (2003), it became necessary to determine if the samples containing alkaloids other than neotuberostemonine had antitussive properties. / The Chinese herb Radix Stemonae (Baibu) has long been used as an antitussive in Chinese medicine for some two thousand years. Its source materials, according to the Pharmacopoeia of the People's Republic of China (PRC Pharmacopoeia), come from the tuberous roots of three Stemona species, namely, S. japonica (Blume) Miq., S. sessilifolia (Miq.) Miq. and S. tuberosa Lour. However, hardly any experimental study is available to document their antitussive functions. Chung et al. (2003) reported that the antitussive components of S. tuberosa were neotuberostemonine and related stenine type Stemona alkaloids. And the antitussive potency of neotuberostemonine through intraperitoneal administration was reported to be comparable to codeine but not involving opioid receptors. In continuation with the study of the antitussive properties of the herb, it was found that total alkaloids of different samples of the herb appeared to vary in chemical profiles, whereas neotuberostemonine was found in only a few samples. / The major components of S. tuberosa including stemoninine, croomine and neotuberostemonine were isolated and determined by spectroscopic methods. It was the first time to isolate croomine from Stemona species, lending support to retaining the two genera Stemona and Croomina in the family Stemonaceae according to chemotaxonomy. Tuberostemonine, another major component of S. tuberosa was also isolated and determined in our team. Neotuberostemonine and tuberostemonine were two isomers but mutually exclusive in our tested samples. Moreover, these major components of S. tuberosa belonged to three types in molecular structure. Stemoninine was stemonamide type, croomine tuberostemospironine type and both neotuberostemonine and tuberostemonine stenine type. These results suggested that antitussive effects of S. tuberosa might be related to the components belonging to these three molecular types. / Xu Yantong. / "March 2006." / Adviser: Paul But. / Source: Dissertation Abstracts International, Volume: 67-11, Section: B, page: 6231. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (p. 137-155). / 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.

Chan Wai-Lung, William. / Thesis submitted in: December 2000. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (leaves 124-131). / Abstracts in English and Chinese. / Abstract --- p.i / Abstract (Chinese Version) --- p.iii / Acknowledgements --- p.v / Table of Contents --- p.vi / List of Tables --- p.ix / List of Figures --- p.xii / List of Abbreviations --- p.xvi / Chapter 1 --- Introduction --- p.1 / Literature Review --- p.4 / Chapter 1.1 --- A Brief Introduction of Cancer --- p.4 / Chapter 1.2 --- Natural Products as a Drug --- p.5 / Chapter 1.2.1 --- Development of terrestrial plants as a drug --- p.6 / Chapter 1.2.1.1 --- Anticancer drugs from terrestrial plants and Chinese medicinal herbs --- p.7 / Chapter 1.2.2 --- Development of marine organisms as a drug --- p.8 / Chapter 1.2.2.1 --- Anticancer drugs from marine organisms --- p.9 / Chapter 1.3 --- Anticlastogenic Study - an Anticancer Study --- p.10 / Chapter 1.3.1 --- Anticlastogenesis mechanisms study --- p.11 / Chapter 1.3.2 --- In vivo anticlastogenic study --- p.13 / Chapter 1.4 --- Anticlastogenic Study of Chinese Medicinal Herbs and Marine Algae --- p.17 / Chapter 1.4.1 --- Selection of nine Chinese medicinal herbs and three marine algae for anticlastogenic screening --- p.18 / Chapter 1.5 --- Methods of Investigation --- p.20 / Chapter 1.5.1 --- Extraction methods --- p.20 / Chapter 1.5.2 --- Single cell gel electrophoresis (Comet assay) --- p.21 / Chapter 2 --- Materials and Methods --- p.27 / Chapter 2.1 --- Materials --- p.27 / Chapter 2.1.1 --- Chinese medicinal herbs --- p.27 / Chapter 2.1.2 --- Marine algae --- p.27 / Chapter 2.1.3 --- Animals --- p.27 / Chapter 2.1.4 --- Chemicals and solutions --- p.28 / Chapter 2.2 --- Methods --- p.31 / Chapter 2.2.1 --- Crude extraction of natural products --- p.31 / Chapter 2.2.1.1 --- Water extraction of Chinese herbs --- p.31 / Chapter 2.2.1.2 --- Water extraction of marine algae --- p.31 / Chapter 2.2.2 --- Test for the effective dosage of clastogen ethyl methanesulfonate (EMS) to BALB/c mice --- p.31 / Chapter 2.2.2.1 --- In vitro test --- p.32 / Chapter 2.2.2.2 --- In vivo test --- p.32 / Chapter 2.2.3 --- Anticlastogenic bioassays --- p.33 / Chapter 2.2.3.1 --- In vitro anticlastogenic screening --- p.33 / Chapter 2.2.3.2 --- In vitro anticlastogenic mechanisms investigation --- p.33 / Chapter 2.2.3.3 --- In vivo anticlastogenic screening --- p.34 / Chapter 2.2.3.4 --- Different in vivo anticlastogenic treatment schedules --- p.35 / Chapter 2.2.4 --- Single cell gel electrophoresis assay (Comet assay) --- p.36 / Chapter 2.2.5 --- White blood cell viability determination --- p.37 / Chapter 2.2.6 --- Statistical analysis --- p.38 / Chapter 3 --- Results --- p.40 / Chapter 3.1 --- Extraction amount of different natural products and cell viability checking --- p.40 / Chapter 3.1.1 --- Chinese medicinal herbs --- p.40 / Chapter 3.1.2 --- Seaweeds --- p.40 / Chapter 3.1.3 --- Cell viability --- p.42 / Chapter 3.2 --- Effective dosage of clastogen EMS to BALB/c mice peripheral white blood cells --- p.42 / Chapter 3.2.1 --- In vitro --- p.42 / Chapter 3.2.2 --- In vivo --- p.42 / Chapter 3.3 --- In vitro anticlastogenic screen test and mechanisms investigation --- p.44 / Chapter 3.3.1 --- In vitro anticlastogenic screen test --- p.44 / Chapter 3.3.1.1 --- Chinese herbs --- p.44 / Chapter 3.3.1.2 --- Seaweeds --- p.53 / Chapter 3.3.2 --- In vitro anticlastogenic mechanisms investigation --- p.55 / Chapter 3.3.2.1 --- H. dilatata --- p.56 / Chapter 3.3.2.2 --- S. angustifolium --- p.56 / Chapter 3.3.2.3 --- S. siliquastrum --- p.63 / Chapter 3.4 --- In vivo anticlastogenic screen test and mechanisms investigation --- p.66 / Chapter 3.4.1 --- In vivo anticlastogenic screen test --- p.66 / Chapter 3.4.1.1 --- Chinese herbs --- p.66 / Chapter 3.4.1.2 --- Seaweeds --- p.73 / Chapter 3.4.2 --- Different treatment methods in in vivo anticlastogenic test --- p.86 / Chapter 3.4.2.1 --- Simultaneous application method --- p.86 / Chapter 3.4.2.2 --- Pre-drug treatment method --- p.91 / Chapter 3.4.2.3 --- Post drug treatment method --- p.91 / Chapter 4 --- Discussion --- p.94 / Chapter 4.1 --- Cell viability and water extracts in Chinese medicinal herbs and marine algae --- p.94 / Chapter 4.2 --- Clastogenic effect of EMS to pWBCs of BALB/c mice --- p.94 / Chapter 4.3 --- In vitro anticlastogenic screen test of nine water extracts of Chinese medicinal herbs and three water extracts of marine algae --- p.99 / Chapter 4.4 --- In vitro anticlastogenic mechanisms investigation of three \03 marine algae extracts --- p.103 / Chapter 4.5 --- In vivo anticlastogenic screen test of Chinese herbs extracts and seaweeds extracts --- p.108 / Chapter 4.6 --- Different administration methods in in vivo anticlastogenic test --- p.115 / Chapter 4.6.1 --- Intraperitoneal route of administration --- p.115 / Chapter 4.6.2 --- In vivo pre- and post-treatment methods --- p.116 / Chapter 5 --- Summary and Conclusion --- p.120 / References --- p.124

Wong, Ka Yee. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 177-189). / Abstracts in English and Chinese; includes Chinese. / Abstract --- p.i / 摘要 --- p.iii / Acknowledgements --- p.v / Table of Contents --- p.vii / List of Appendices --- p.xi / List of Tables --- p.xii / List of Figures --- p.xiv / Abbreviations --- p.xvi / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- General Introduction --- p.1 / Chapter 1.2 --- Background to the study --- p.2 / Chapter 1.2.1 --- Epidemiology of cancer --- p.2 / Chapter 1.2.1.1 --- Incidence and mortality in the World --- p.2 / Chapter 1.2.1.2 --- Incidence and mortality in Hong Kong --- p.4 / Chapter 1.2.2 --- Prevalence of Traditional Chinese Medicine (TCM) --- p.5 / Chapter 1.2.3 --- Prevalence of Traditional Chinese Medicine (TCM) in cancer --- p.6 / Chapter 1.2.4 --- Development of TCM in Hong Kong --- p.7 / Chapter 1.3 --- Theoretical rationale of the study --- p.8 / Chapter 1.4 --- Significance of the study --- p.11 / Chapter Chapter 2 --- Literature Review --- p.13 / Chapter 2.1 --- Introduction --- p.13 / Chapter 2.2 --- The concept of Advanced Cancer --- p.13 / Chapter 2.2.1 --- Pathology of Advanced Cancer --- p.14 / Chapter 2.2.1.1 --- Metastatic Cancer --- p.14 / Chapter 2.2.2 --- Sign and Symptoms of Advanced Cancer --- p.19 / Chapter 2.2.3 --- Diagnosis of Advanced Cancer --- p.19 / Chapter 2.2.4 --- Current Treatment for Advanced Cancer --- p.21 / Chapter 2.2.5 --- Limitation of Current Treatments --- p.24 / Chapter 2.3 --- Diagnosis and Treatment by TCM of Advanced Cancer --- p.26 / Chapter 2.3.1 --- (Advanced) Cancer from the TCM perspectives --- p.26 / Chapter 2.3.2 --- Diagnosis by TCM of Advanced Cancer --- p.27 / Chapter 2.3.3 --- Treatment by TCM of Advanced Cancer --- p.28 / Chapter 2.4 --- Current Evidences about the Clinical Effectiveness of TCM on Cancer Patients --- p.29 / Chapter 2.5 --- The concept of Health-related Quality of Life (HRQOL) --- p.35 / Chapter 2.5.1 --- The importance of HRQOL to cancer patients --- p.35 / Chapter 2.5.2 --- HRQOL instruments --- p.37 / Chapter 2.5.2.1 --- EORTC QLQ-C30 --- p.38 / Chapter 2.5.2.2 --- SF-36 --- p.39 / Chapter 2.6 --- Summary of Literature Review --- p.40 / Chapter 2.7 --- The research questions --- p.41 / Chapter 2.8 --- Research Hypotheses --- p.42 / Chapter 2.9 --- The design of TCM protocol --- p.42 / Chapter Chapter 3 --- Methodology --- p.45 / Chapter 3.1 --- Introduction --- p.45 / Chapter 3.2 --- Protocol --- p.45 / Chapter 3.2.1 --- Study Design --- p.46 / Chapter 3.2.2 --- Selection of Participants --- p.46 / Chapter 3.2.2.1 --- Inclusion criteria --- p.48 / Chapter 3.2.2.2 --- Exclusion criteria --- p.49 / Chapter 3.2.3 --- Sample size calculation --- p.50 / Chapter 3.2.4 --- Setting --- p.51 / Chapter 3.2.5 --- Interventions --- p.51 / Chapter 3.2.5.1 --- Treatment --- p.51 / Chapter 3.2.5.2 --- Medication and dose/dosage --- p.52 / Chapter 3.2.5.3 --- Treatment Assignment --- p.55 / Chapter 3.2.5.4 --- Concurrent Medications --- p.56 / Chapter 3.2.6 --- Procedure and Methods --- p.56 / Chapter 3.2.6.1 --- Informed Consent --- p.56 / Chapter 3.2.6.2 --- Documentation --- p.57 / Chapter 3.2.6.3 --- Assessment Procedure --- p.57 / Chapter 3.2.7 --- Outcome Measurements --- p.62 / Chapter 3.2.7.1 --- Survey Questionnaire --- p.62 / Chapter 3.2.7.2 --- Quality of life (QOL) instruments --- p.62 / Chapter 3.2.7.3 --- Global Ratings --- p.64 / Chapter 3.2.7.4 --- Physical Examination and Laboratory tests --- p.65 / Chapter 3.2.8 --- Safety Considerations --- p.66 / Chapter 3.2.8.1 --- Adverse Events (AE) --- p.66 / Chapter 3.2.8.2 --- Serious Adverse Event (SAE) --- p.66 / Chapter 3.2.8.3 --- Causality Assessment --- p.67 / Chapter 3.2.9 --- Ethical consideration --- p.68 / Chapter 3.2.10 --- Data Collection --- p.69 / Chapter 3.3 --- Data analysis --- p.69 / Chapter 3.4 --- Expected Outcomes of Study --- p.71 / Chapter Chapter 4 --- Results --- p.72 / Chapter 4.1 --- Study Progress --- p.72 / Chapter 4.2 --- The Participants --- p.72 / Chapter 4.3 --- Clinical characteristics and Socio-demographics of Participants --- p.75 / Chapter 4.4 --- Main Outcome - Quality of Life --- p.78 / Chapter 4.4.1 --- QLQ-C30 --- p.79 / Chapter 4.4.1.1 --- Scoring and Transforming of items into scales --- p.79 / Chapter 4.4.1.2 --- Changes of Individual Scale at Different Visits --- p.80 / Chapter 4.4.1.3 --- Clinical significance of Scales --- p.98 / Chapter 4.4.2 --- SF-36 --- p.104 / Chapter 4.4.2.1 --- Scoring and Transforming of items into scales --- p.104 / Chapter 4.4.2.2 --- Changes of Individual Scale at Different Visits --- p.104 / Chapter 4.4.2.3 --- SF-36 Summary Scales --- p.113 / Chapter 4.4.3 --- Correlation of QLQ-C30 and SF-36 --- p.115 / Chapter 4.5 --- Measurement of Physical examination --- p.117 / Chapter 4.5.1 --- Body Weight --- p.117 / Chapter 4.6 --- Measurement of Laboratory Blood tests --- p.118 / Chapter 4.6.1 --- "Comparison of CBC, RFT, LFT and LD" --- p.118 / Chapter 4.6.2 --- Tumor Markers --- p.120 / Chapter 4.7 --- Adverse Events and Serious Adverse Events --- p.121 / Chapter 4.8 --- Global Ratings --- p.123 / Chapter 4.8.1 --- Global Rating 1 - Severity of Disease --- p.123 / Chapter 4.8.2 --- Global Rating 2 - Global Disease Status --- p.124 / Chapter 4.8.2.1 --- Change in Global Disease Status --- p.125 / Chapter 4.8.2.2 --- Agreement between RCMP and clinician --- p.125 / Chapter 4.8.2.3 --- Patients' perception after treatment --- p.126 / Chapter 4.9 --- Distribution of TCM patterns and Chinese herbal medicines --- p.127 / Chapter 4.10 --- Survival Rate --- p.132 / Chapter 4.11 --- Conclusion --- p.133 / Chapter Chapter 5 --- Discussion --- p.135 / Chapter 5.1 --- Conclusion on findings --- p.135 / Chapter 5.2 --- Baseline profile of participants --- p.137 / Chapter 5.3 --- Feasibility of TCM on advanced cancer patients --- p.139 / Chapter 5.3.1 --- Recruitment of Participants --- p.139 / Chapter 5.3.2 --- Compliance of participants to the study schedule --- p.140 / Chapter 5.4 --- Health-related Quality of Life --- p.142 / Chapter 5.5 --- Safety of TCM --- p.149 / Chapter 5.6 --- Chinese medicine practitioner vs Western medicine doctor --- p.150 / Chapter 5.7 --- TCM pattern differentiation and treatment --- p.151 / Chapter 5.8 --- Implication of study --- p.154 / Chapter 5.8.1 --- Clinical implication --- p.154 / Chapter 5.8.2 --- Policy implication --- p.154 / Chapter 5.9 --- Limitations of the study --- p.155 / Chapter 5.10 --- Recommendations for further studies --- p.157 / Chapter 5.11 --- Overall Conclusion --- p.158 / Appendices --- p.160 / References --- p.177

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

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