This was a chemical laboratory study. The main focus was to evaluate the chemical stability of Hypericum perforatum (St John's wort), Ginkgo biloba and Piper methysticum (Kava Kava) under unfavourable environmental conditions. Different dosage forms representing the same amount of active ingredients for each were used. Some of the dosage forms were self manufactured according to Good Manufacturing Practice. Samples of the dried powder of each plant was also exposed to a series of gamma¬radiation. Acetone was used as an extractant for all three plants, after evaluating and discarding the extraction method stipulated in the British Herbal Pharmacopoeia. Identification of the different plants were carried out by means of Thin Layer Chromatography. The in-house developed mobile phases EMW, BEA and CEF, showed better separation and visibility compared to the mobile phases used in the British Herbal Pharmacopoeia. The plates were sprayed with either vanillin or p-anisaldehide for optimal visualization of the separated compounds. After the specified period of 6-months, comparative TLC was performed on all samples. This was achieved for each plant by applying all samples stored at a specific condition i.e.25°C, on the same plate. The samples were stored at low temperature after exposure to the specific time interval. Quantitative analysis was performed by spectrophotometry, and high pressure liquid chromatography. The data obtained from these analytical methods, were used to evaluate the relative chemical stability of each dosage form. The relationship between the quantitative data and the qualitative changes in the TLC fingerprints, were compared, hoping to achieve a common pattern relating to the stability. The order of the reaction as well as the reaction rate constant (k) for each dosage form was calculated, except for kava kava. The shelf-life (too) was calculated using the analyzed data obtained by spectrophotometry or HPLC. The relevance of conventional pharmaceutical calculations in the prediction of shelf-life, by means of accelerated stability tests, was investigated for the possible application to herbal products. The effects of gamma radiation on the degradation of the chemical compounds present in each plant, was evaluated. After an evaluation of all the relevant data, it seemed that the tablet-dosage forms were equally effective regarding stability, compared to the capsules. Liquid extracts appeared to be less stable than the extract capsules. The extract capsules seemed to degrade more rapidly than the herbal tablets or herbal capsules. Exposure to low dose radiation (4.4 kGy) did not seem to have an influence on the stability. It was evident that some herbs were more sensitive to sunlight or heat than others. In general, all three of the chosen plants seemed to be relatively stable if stored in the specified conditions. It seemed valid for the shelf-life to be expressed as two years. / Dissertation (MSc (Pharmacology))--University of Pretoria, 2001. / Pharmacology / unrestricted

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

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

Lee, Kit Lin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 95-105). / Abstracts in English and Chinese. / Abstract --- p.i / 撮要 --- p.iii / Acknowledgements --- p.v / Table of contents --- p.vii / List of Tables --- p.x / List of Figures --- p.xi / List of Abbreviations --- p.xiii / Chapter Chapter 1: --- Literature Review --- p.1 / Chapter 1.1 --- Introduction --- p.1 / Chapter 1.1.1 --- History of Botanical Studies in Hong Kong --- p.1 / Chapter 1.1.2 --- Plant Species Named after Hong Kong --- p.2 / Chapter 1.2 --- Botanical Background of Asarum Plants --- p.5 / Chapter 1.2.1 --- Plant Species under the Family of Aristolochiaceae --- p.5 / Chapter 1.2.2 --- Herba Asari --- p.6 / Chapter 1.2.3 --- Classification of Asarum hongkongense --- p.8 / Chapter 1.2.4 --- Growing Habitat of Asarum hongkongense --- p.8 / Chapter 1.3 --- Medicinal Properties of Asari --- p.10 / Chapter 1.4 --- Chemical Constituents of Asari --- p.10 / Chapter 1.5 --- Aristolochic acid and Health Issues --- p.12 / Chapter 1.5.1 --- Aristolochic Acid Intoxication --- p.12 / Chapter 1.5.2 --- Description of Aristolochic Acid --- p.13 / Chapter 1.5.3 --- Toxicities of Aristolochic Acid --- p.13 / Chapter 1.5.4 --- Aristolochic Acid-Containing Plants --- p.15 / Chapter 1.5.5 --- Control of Aristolochic Acid-Containing Products --- p.17 / Chapter 1.5.6 --- Control of Aristolochic Acid-Containing Products in Hong Kong --- p.18 / Chapter 1.6 --- Objectives of Study --- p.19 / Chapter Chapter 2: --- Macroscopic Features of Asarum hongkongense --- p.20 / Chapter 2.1 --- Introduction --- p.20 / Chapter 2.2 --- Plant Material --- p.20 / Chapter 2.2.1 --- Asarum hongkongense --- p.20 / Chapter 2.2.2 --- Herba Asari --- p.23 / Chapter 2.3 --- Macroscopic Characteristics of Aarum hongkongense --- p.23 / Chapter 2.3.1 --- Leaf --- p.23 / Chapter 2.3.2 --- Root and Rhizome --- p.25 / Chapter 2.3.3 --- Flower --- p.27 / Chapter 2.4 --- Macroscopic Characteristics of Herba Asari heterotropoidis (Liaoxixin) --- p.31 / Chapter 2.4.1 --- Leaf --- p.31 / Chapter 2.4.2 --- Root and Rhizome --- p.31 / Chapter 2.4.3 --- Flower --- p.34 / Chapter 2.5 --- Discussion --- p.36 / Chapter Chapter 3: --- Microscopic Features of Asarum hongkongense --- p.38 / Chapter 3.1 --- Introduction --- p.38 / Chapter 3.2 --- Plant Materials --- p.39 / Chapter 3.3 --- "Chemical,Reagents and Instrumentation" --- p.39 / Chapter 3.4 --- Methods --- p.39 / Chapter 3.5 --- Microscopic Characteristics of Asarum hongkongense --- p.40 / Chapter 3.5.1 --- Transverse Section of Leaf --- p.40 / Chapter 3.5.2 --- Surface View of Leaf --- p.40 / Chapter 3.5.3 --- Transverse Section of Root --- p.43 / Chapter 3.5.4 --- Transverse Section of Rhizome --- p.43 / Chapter 3.5.5 --- Powder --- p.47 / Chapter 3.5.5.1 --- Pollens --- p.47 / Chapter 3.5.5.2 --- Vessels --- p.47 / Chapter 3.5.5.3 --- Starch Grains --- p.47 / Chapter 3.6 --- Microscopic Characteristics of Herba Asari heterotropoidis (Liaoxixin) --- p.49 / Chapter 3.6.1 --- Transverse Section of Leaf --- p.49 / Chapter 3.6.2 --- Surface View of Leaf --- p.49 / Chapter 3.6.3 --- Transverse Section of Root --- p.53 / Chapter 3.6.4 --- Transverse Section of Rhizome --- p.53 / Chapter 3.6.5 --- Powder --- p.56 / Chapter 3.6.5.1 --- Starch Grains --- p.56 / Chapter 3.6.5.2 --- Vessels --- p.56 / Chapter 3.7 --- Discussion --- p.58 / Chapter Chapter 4: --- Molecular DNA Sequencing of Asarum hongkongense --- p.61 / Chapter 4.1 --- Introduction --- p.61 / Chapter 4.2 --- Sample Preparation --- p.64 / Chapter 4.3 --- Method --- p.64 / Chapter 4.3.1 --- Extraction of Total DNA --- p.64 / Chapter 4.3.2 --- PCR Amplification of ITS1 and ITS2 Regions of rRNA Gene --- p.65 / Chapter 4.3.3 --- Purification of PCR Products --- p.65 / Chapter 4.3.4 --- Sequencing of ITS Regions --- p.66 / Chapter 4.3.4.1 --- Cycle Sequencing Reaction --- p.66 / Chapter 4.3.4.2 --- Purification of Sequencing Extension Products --- p.67 / Chapter 4.3.4.3 --- Electrophoresis by Genetic Analyzer --- p.67 / Chapter 4.3.4.4 --- Sequence Analysis and Alignment --- p.67 / Chapter 4.4 --- Results and Discussion --- p.68 / Chapter 4.4.1 --- Extraction of Total DNA --- p.68 / Chapter 4.4.2 --- PCR Amplification of ITS1 and ITS2 Regions of rRNA Gene --- p.68 / Chapter 4.4.3 --- Sequence Analyses --- p.68 / Chapter Chapter 5: --- Determination of Aristolochic Acid of Asarum hongkongense --- p.80 / Chapter 5.1 --- Introduction --- p.80 / Chapter 5.2 --- Sample Preparation --- p.81 / Chapter 5.3 --- Standard Preparation --- p.81 / Chapter 5.4 --- Experimental --- p.83 / Chapter 5.4.1 --- Chemical and Reagents --- p.83 / Chapter 5.4.2 --- Methods --- p.83 / Chapter 5.4.2.1 --- High-Performance Liquid Chromatography --- p.83 / Chapter 5.4.2.2 --- Mass Spectrometry --- p.85 / Chapter 5.4.3 --- Other Instrumentation --- p.85 / Chapter 5.5 --- Method Validation --- p.85 / Chapter 5.5.1 --- Calibration --- p.85 / Chapter 5.5.2 --- Precision --- p.87 / Chapter 5.5.3 --- Recovery Test --- p.88 / Chapter 5.5.4 --- Limit of Detection --- p.89 / Chapter 5.6 --- Results and Discussion --- p.90 / Chapter Chapter 6: --- Conclusion --- p.92 / References --- p.94

Submitted in complete fulfillment for the Degree of Master of Technology: Biotechnology, Durban University of Technology, 2012. / Recently our understanding of cancer has advanced in the realization that apoptosis and the genes that control it have a profound effect on the malignant phenotype. It is now clear that some oncogenic mutations disrupt apoptosis, leading to tumor initiation, progression or metastasis. Conversely, compelling evidence indicates that other oncogenic changes promote apoptosis, thereby producing selective pressure to override apoptosis during multistage carcinogenesis. Finally, it is now well documented that most cytotoxic anti-cancer agents induce apoptosis, raising the intriguing possibility that defects in apoptotic programs contribute to treatment failure. Because the same mutations that suppress apoptosis during tumor development also reduce treatment sensitivity, apoptosis provides a conceptual framework to link cancer genetics with cancer therapy. An intense research effort is uncovering the underlying mechanisms of apoptosis, such that, in the next decade, one envisions that this information will produce new strategies to exploit apoptosis for therapeutic benefit. Plants have a long history in cancer treatment. More than 3000 species have been known for their anti-cancer potential. Over 60% of currently used anti-cancer agents are derived in one way or another from higher plants. Indeed, compounds derived from natural sources, including plants, have played, and continue to play, a dominant role in the discovery of leads for the development of conventional drugs for the treatment of most human diseases especially cancer. Thus the aim of this study was to investigate if Centella asiatica and Elytropappus rhinocerotis possess anti-cancer potential and determine the effect on the modulation of apoptosis. In South Africa C. asiatica is known anecdotally to treat various forms of cancers and E. rhinocerotis is known to treat colic and diarrhoea. The anti-cancer activity of C. asiatica has been studied in some parts India but E. rhinocerotis has not been investigated. This study was conducted using polarity guided fractionation (aqueous, ethanolic, methanolic and hexane), thereafter these extracts were tested for their toxicity on a colon cancer cell line (CaCO-2) and on normal cells vi (PBMC). Subsequently, the most active extract was used to isolate the active fraction. The fraction that displayed toxicity on the CaCO-2 cells were further investigated for their ability to induce apoptosis by observing the morphological effects and DNA changes using acridine orange-ethidium bromide staining. Apoptosis was confirmed using Annexin V- PI staining. Nuclear effects were studied by DNA fragmentation and by agarose gel electrophoresis. Nuclear fragmentation was studied by flow cytometry using bromodeoxyuridine (BrDU). Pro-apoptotic changes were determined with Caspase III enzyme levels using flow cytometry. The results were compared to the effect of a known anti-carinogen - Taxol. The anti-oxidant activity was also evaluated for the different extracts. The ethanolic extracts of both C. asiatica and E. rhinocerotis showed more than 100% radical scavenging activity. The methanolic extract (125 μg/ml -500 μg/ml) showed cytotoxicity on the CaCO-2 cells and a proliferative effect on the PBMC. Apoptosis was confirmed in the methanolic extract for both plants and was therefore used to carry forth this study. This included early apoptotic changes observed by the morphological study i.e., membrane blebbing, nuclear condensation and the presence of apoptotic bodies, in both C. asiatica and E. rhinocerotis fractions demonstrated more non-viable apoptotic cells than the methanolic extracts. Late changes of apoptosis were also found as indicated by DNA laddering and a positive outcome with BrDU. Both the active fractions from C. asiatica and E. rhinocerotis showed more DNA laddering and active caspase III than the methanolic extract. These features indicate that C. asiatica and E. rhinocerotis cause apoptotic death of colon cancer cells CaC0-2. In conclusion, there was a significant increase in apoptosis of CaCO-2 cells with little alteration of PBMC in the presence of the methanolic extract of C. asiatica and E. rhinocerotis. The semipure fractions resulted in changes related to late apoptosis. The results suggest that C. asiatica and E. rhinocerotis induces apoptosis in CaCO-2 cells which is an important step in elucidating the underlying molecular mechanism for anti-tumour activity.

Submitted in partial compliance with the requirements of the Master’s Degree in Technology: Homoeopathy, Durban University of Technology, Durban, South Africa, 2016, / Background Diabetes mellitus is a metabolic disorder with various aetiologies, characterised by hyperglycaemia, resulting from defects of carbohydrate, fat and protein metabolism due to the deficient action of insulin on target tissues caused by insensitivity to or lack of insulin or both. The long term effects of diabetes mellitus frequently include retinopathy, nephropathy and neuropathy and an increased risk of other diseases such as cardiac, peripheral arterial and cerebrovascular disease. According to the International Diabetes Federation (IDF) 387 million people have diabetes mellitus and this number is predicted to rise to 592 million worldwide by 2035. In 2014 diabetes mellitus caused 4.9 million deaths worldwide and every 7 seconds a person dies from diabetes mellitus. The growing incidence of diabetes mellitus is a worldwide concern because of the increase of economic costs and burden of disease that is due to the cardiovascular complications and the co-morbidities. Objective The aim of this double-blind, randomised clinical trial was to determine the efficacy of Syzygium jambolanum (Java plum) 6CH and Syzygium jambolanum (Java plum) homoeopathic mother tincture on daily fasting blood glucose and glycosylated haemoglobin levels in type 2 diabetes mellitus patients on Metformin® in the treatment of type 2 diabetes mellitus. Material and Method A sample consisted of 24 volunteers selected on the basis of inclusion and exclusion criteria. These participants were then randomly divided into two groups, 13 in the group receiving the homoeopathic potency and 11 in the group receiving the homoeopathic mother tincture. Each participant attended a total of five consultations with the researcher over a period of 14 weeks that included a 2 week baseline period followed by a 12 week treatment period, at the Durban University of Technology (DUT) or Kenneth Gardens Homoeopathic Day Clinic. At each consultation a detailed and comprehensive homoeopathic case history (Appendix D) was taken and a physical examination (Appendix E) was performed by the researcher. Participants were required to fill in a log sheet (Appendix C1 and C2) with their fasting blood glucose readings daily for 14 weeks, which included a 2 week baseline period followed by a 12 week treatment period. Participants were also required to have their glycosylated haemoglobin measurements tested pre- and post-treatment. Results Both groups reflected a statistically significant reduction in fasting blood glucose levels as compared to the baseline. The mean fasting blood glucose level in week 1 was 11.8802 whereas in week 13 the mean blood glucose level was 8.6590 with a p value ≤ 0.05 for the Syzygium jambolanum 6CH group and the mean blood glucose level in week 1 was 9.0338 with a standard whereas in week 13 the mean blood glucose level was 6.8591 with a p value ≤ 0.05 in the Syzygium jambolanum homoeopathic mother tincture. However there was no significant differences between the two groups (Syzygium jambolanum 6CH and Syzygium jambolanum homoeopathic mother tincture), the significance score was 0.623 when comparing reduction in fasting blood glucose levels. Both groups reflected a statistically non-significant reduction in the glycosylated haemoglobin (HbA1C) and there were no significant differences between the two groups when comparing reduction in HbA1C levels. Conclusion Both homoeopathic preparations of Syzygium jambolanum (mother tincture and 6CH) significantly reduce fasting blood glucose levels in patients with type 2 diabetes mellitus. This result suggests that Syzygium jambolanum has beneficial anti-diabetic effects and warrants further investigation. / M

The aim of this thesis was to explore the socio-economic factors that impact on the sustainable harvesting of buchu in the Western Cape of South Africa. Some of the factors that were explored include poverty, natural resource tenure, legislation, and local practices with regard to the harvesting of buchu.

The aim of this study is to isolate and evaluate the anticonvulsant components from the leaves of Leonotis leonorus (L) R.aR. and to see if there is any change in activity with the origin of the plant material and I or the season in which plant material is collected. Therefore, in this study, two sites were chosen for collection of plant material and the collection was made in summer and in winter. Chemical, physical and pharmacological methods were used to isolate, identify and to evaluate compounds isolated from the leaves of Leonotis leonorus for anticonvulsant activity.

All the results showed that TCMs can provide a source for discovering anti-angiogenic agents for the treatment of cancer, and all these experiments in the zebrafish and mammalian models further confirmed the value of zebrafish model in anti-angiogenic drug discovery. / Angiogenesis refers to the formation of new blood capillaries from pre-existing ones, and is essential in a series of normal physiological processes such as embryonic development and pathological responses. However, persistent unregulated angiogenesis causes "angiogenic diseases" such as diabetic retinopathy, tumor growth and metastasis, rheumatoid arthritis, and inflammatory diseases. The linkage between angiogenesis, tumor growth and metastasis was first hypothesized by Dr. Judah Folkman in the 1970s, and now this controversial idea is widely accepted and the inhibition of angiogenesis, or anti-angiogenesis, is considered as a promising anticancer therapeutic strategy. Bevacizumab (Avastin RTM by Genentech Inc.), the first approved anti-angiogenic drug by U.S. FDA in 2004, is a humanized monoclonal antibody to inhibit endothelial cell proliferation and angiogenesis for the treatment of metastatic colorectal cancer, non-small cell lung cancer, advanced breast cancer, glioblastoma, metastatic renal cell cancer. / Anti-angiogenic therapy in cancer treatment has led to the development of compounds designed to control a tumor's growth by blocking its ability to develop a blood supply. The development of agents with different mechanisms of action requires powerful preclinical models for the analysis and optimization of the therapy. Some in vitro and in vivo anti-angiogenic assays are already developed, for example, Human Umbilical Vein Endothelial Cell (HUVEC) assay, Chorioallantoic Membrane assay, Matrigel plug assay et al. Zebrafish, as a relatively new model organism, is firmly established as a powerful research platform for many areas of biology and drug discovery, allowing the testing of bioactive compounds in a whole organism and in cells undergoing normal cell-cell and cell-matrix interactions. Many anti- and pro-angiogenic molecules tested in zebrafish demonstrated similar effects to those observed in humans or other mammalian models. Besides providing a powerful platform for drug screening, zebrafish model can also be used for probing biological processes, and generate insights into mechanisms. / Cancer is a generic term for a large group of diseases that can affect any part of the body, which causes a vast medical problem and is a leading cause of death worldwide nowadays. However, for many years the main methods of treating cancer have been surgery, radiotherapy and chemotherapy. Among these treatments, chemotherapy has played a major role in cancer therapy for half a century. Despite improving managements and efforts, it is not surprising that the prognosis has not greatly improved because of the limitations of current therapies, such as toxicity, inherent and acquired resistance, and metastatic spread. This calls for novel cancer therapies and new group of anticancer agents for selectively targeting cancers without or with lower toxicity to normal tissues. / Traditional Chinese medicines (TCMs) have long been recognized as a rich source for discovering drugs, and various TCMs and their components have shown anti-angiogenic properties. In this thesis study, as a continuing pursuit for elucidating the anti-angiogenic properties of TCMs, our attention is focused on those with effects of anti-inflammation, anti-rheumatoid arthritis and anti-cancer. On zebrafish screening model, three of the selected TCMs, Rheum palmatum, Alpinia oxyphylla (seeds), and Kaempferia galanga showed potential anti-angiogenic activity, indicating the existence of potent anti-angiogenic components in these herbs. The ethyl acetate fraction of R. palmatum showed strong inhibition of vessel formation in zebrafish embryos. Further testing of the anthraquinones of this herb showed three of them displayed potent anti-angiogenic activities. The most potent compound---rhein could inhibit HUVEC migration and affect the mRNA expression of vegfa, kdr, angiopoietin1/2 and tie1/2; The n-hexane and ethyl acetate fractions of A. oxyphylla and K. galangal showed anti-angiogenic potentials both in zebrafish and HUVEC assays. The n-hexane and ethyl acetate fractions of A. oxyphylla could both inhibit the proliferation, migration and tube formation processes of HUVEC. And the most potential component, trans-ethyl-p-methoxycinnamate from K. galanga, could inhibit HUVEC migration and tube formation, and reduce all gene expressions involved in angiogenesis process except for vegfa. / He, Zhiheng. / Adviser: Wei Ge. / Source: Dissertation Abstracts International, Volume: 73-02, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 87-108). / 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.

D. Tech. Pharmaceutical Sciences. / Aims of the research project was to develop and optimise rapid quality control methods for H. gordonii raw material and products. The second aim was to determine whether the perceived active component of H. gordonii (P57) is transported across porcine intestinal and buccal mucosa.