Charles University in Prague Faculty of Pharmacy in Hradec Kralove Department of Social and Clinical Pharmacy The analysis of pharmacotherapy in patients suffering from hyperlipidemia (Diploma Thesis) Mentor of Diploma Thesis Prof. PharmDr. Jiří Vlček, Ph.D. Mavrovouniotis Konstantinos- Parmenion Hradec Králové 2015 ABSTRACT ENGLISH The analysis of pharmacotherapy in patients suffering from hyperlipidemia Mavrovouniotis Konstantinos Mentor: Prof. Dr. Jiří Vlček, CSc. Introduction: Hyperlipidemia is a serious condition whereby the blood levels of lipids, cholesterol and triglycerides are abnormally elevated. This condition is generally asymptomatic but may lead to atherosclerotic heart disease and other types of cardiovascular pathology if not treated effectively. Various risk factors can affect the onset and severity of hyperlipidemia and those include genetic predisposition, hypertension, diabetes mellitus, obesity, poor diet, lack of regular exercise, smoking etc. Measurement and monitoring of blood levels of triglycerides, cholesterol and lipoproteins can be used as prevention method for assessing the risk for an individual to develop hyperlipidemia. Once a patient is diagnosed with the condition several approaches exist for the treatment. The main goal of the treatment is to reduce the risk of...

Yeung Chi Hang, Thomas. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves 126-146). / Abstracts in English and Chinese. / Table of content / ACKNOWLEDGEMENT --- p.i / ABSTRACT --- p.ii / LIST OF ABBREVIATION --- p.vi / TABLE OF CONTENTS --- p.vii / Chapter Chapter1 --- General Introduction / Chapter 1.1 --- INTRODUCTION --- p.1 / Chapter 1.2 --- FORMATION OF CLA --- p.1 / Chapter 1.3 --- OCCURRENCE OF CLA IN FOODS --- p.5 / Chapter 1.4 --- PHYSIOLOGICAL EFFECTS OF CLA --- p.8 / Chapter 1.4.1 --- Anticarcinogenic Effects of CLA --- p.8 / Chapter 1.4.2 --- Antiatherogenic Effect of CLA --- p.11 / Chapter 1.4.3 --- Antioxidant Effect of CLA --- p.12 / Chapter 1.4.4 --- CLA and Immune Response --- p.13 / Chapter 1.4.5 --- CLA and Body Composition --- p.14 / Chapter Chapter2 --- Protective Effect of CLA on Copper-Induced Human LDL Oxidation / Chapter 2.1 --- INTRODUCTION --- p.17 / Chapter 2.1.1 --- Oxidative Modification of LDL and Atherosclerosis --- p.20 / Chapter 2.1.1.1 --- Understanding of LDL --- p.20 / Chapter 2.1.1.2 --- Oxidative Modification of LDL --- p.20 / Chapter 2.1.1.3 --- Role of Oxidative Modified LDL in Atherogenesis --- p.23 / Chapter 2.1.2 --- Antioxidants and Atherosclerosis --- p.25 / Chapter 2.1.3 --- Measuring TBARS Formation as an in vitro Index to Monitor LDL Oxidation --- p.26 / Chapter 2.1.4 --- CLA and Atherogenesis --- p.27 / Chapter 2.2 --- OBJECTIVE OF THE PRESENT STUDY --- p.28 / Chapter 2.3 --- MATERIALS AND METHODS --- p.29 / Chapter 2.3.1 --- Human LDL Isolation --- p.29 / Chapter 2.3.2 --- LDL Oxidation --- p.30 / Chapter 2.3.3 --- Thiobarbituric Acid Reactive Substances (TBARS) Assay --- p.30 / Chapter 2.4 --- STATISTICS --- p.31 / Chapter 2.5 --- RESULTS --- p.32 / Chapter 2.5.1 --- Inhibitory Effect of BSA on Human LDL Oxidation --- p.32 / Chapter 2.5.2 --- Pro-oxidant Effect of LA on Human LDL Oxidation --- p.32 / Chapter 2.5.3 --- Inhibitory Effect of CLA on Human LDL Oxidation --- p.32 / Chapter 2.6 --- DISCUSSION --- p.37 / Chapter 2.6.1 --- Effect ofBSA on Copper-Induced LDL Oxidation --- p.37 / Chapter 2.6.2 --- Effect of LA on Copper-Induced LDL Oxidation --- p.38 / Chapter 2.6.3 --- Protective Effect of CLA on Copper-Induced Human LDL Oxidation --- p.39 / Chapter Chapter3 --- Hypolipidemic Activity of CLA / Chapter 3.1 --- INTRODUCTION --- p.42 / Chapter 3.1.1 --- Total Cholesterol and LDL Cholesterol --- p.42 / Chapter 3.1.2 --- Triglyceride (TG) --- p.44 / Chapter 3.1.3 --- Hypolipidemic Effect of CLA --- p.45 / Chapter 3.1.4 --- Golden Syrian Hamster as an Animal Model of Cholesterol Metabolism --- p.46 / Chapter 3.2 --- OBJECTIVES OF THE PRESENT STUDY --- p.48 / Chapter 3.3 --- MATERIALS AND METHODS --- p.48 / Chapter 3.3.1 --- LA and CLA --- p.49 / Chapter 3.3.2 --- Animals --- p.49 / Chapter 3.3.3 --- Experiment1 --- p.49 / Chapter 3.3.4 --- Experiment2 --- p.51 / Chapter 3.3.5 --- "Determination of Serum TC, HDL-Cholesterol (HDL-C) and TG" --- p.54 / Chapter 3.3.6 --- Lipid analysis of Liver and Adipose Tissue --- p.54 / Chapter 3.3.6.1 --- Lipid Extraction and Separation of Different Lipid Species --- p.54 / Chapter 3.3.6.2 --- Acid-Catalyzed Methylation of Fatty Acids --- p.55 / Chapter 3.3.6.3 --- GLC Analysis of FAME --- p.55 / Chapter 3.3.7 --- Quantification of Tissue Cholesterol --- p.56 / Chapter 3.3.7.1 --- Cholesterol Extraction and Silylation --- p.56 / Chapter 3.3.7.2 --- GLC Analysis of TMS-Ether Derivative of Cholesterol --- p.56 / Chapter 3.4 --- STATISTICS --- p.57 / Chapter 3.5 --- RESULTS --- p.59 / Chapter 3.5.1 --- Body Weight and Food Intake --- p.59 / Chapter 3.5.2 --- "Effect of Dietary CLA Supplementation on Serum TG, TC and HDL-C" --- p.59 / Chapter 3.5.3 --- "Effect of Dietary CLA Supplementation on Hepatic TG, Phospholipid and Cholesterol" --- p.64 / Chapter 3.5.4 --- Effect of Dietary CLA Supplementation on Adipose Tissue TG and Cholesterol --- p.73 / Chapter 3.5.5 --- Effect of CLA Supplementation on Cholesterol Levels of Different Tissues --- p.73 / Chapter 3.6 --- DISCUSSION --- p.79 / Chapter 3.6.1 --- "Effect of CLA Supplementation on Serum TG, TC and HDL-C" --- p.79 / Chapter 3.6.2 --- "Effect of CLA Supplementation on Hepatic TG, PL and Cholesterol" --- p.81 / Chapter 3.6.3 --- Effect of CLA on Adipose Tissue TG and Cholesterol --- p.83 / Chapter 3.6.4 --- Implication of CLA Intake in Humans --- p.84 / Chapter Chapter4 --- Influences of Dietary CLA on Cholesterol Homeostasis / Chapter 4.1 --- INTRODUCTION --- p.86 / Chapter 4.2 --- NEUTRAL EFFECT OF DIETARY CLA SUPPLEMENTATION ON HMG-COA REDUCTASE ACTIVITY --- p.88 / Chapter 4.2.1 --- HMG-CoA Reductase as the Rate-Limiting Enzyme in Cholesterol Synthesis --- p.88 / Chapter 4.2.2 --- Objective of The Present Study --- p.91 / Chapter 4.2.3 --- Materials and Methods --- p.92 / Chapter 4.2.3.1 --- Preparation of Hepatic Microsome --- p.92 / Chapter 4.2.3.2 --- HMG-GoA Reductase Activity Assay --- p.92 / Chapter 4.2.4 --- Statistics --- p.93 / Chapter 4.2.5 --- Results --- p.94 / Chapter 4.2.6 --- Discussion --- p.96 / Chapter 4.3 --- DOWN-REGULATION OF THE INTESTINAL ACAT ACTIVITY BY CLA FEEDING --- p.97 / Chapter 4.3.1 --- Role of ACAT in Cholesterol Absorption --- p.97 / Chapter 4.3.2 --- Objective of The Present Study --- p.99 / Chapter 4.3.3 --- Materials and Methods --- p.100 / Chapter 4.3.3.1 --- Preparation of Intestinal Microsome --- p.100 / Chapter 4.3.3.2 --- ACAT Activity Assay --- p.100 / Chapter 4.3.4 --- Statistics --- p.101 / Chapter 4.3.5 --- Results --- p.102 / Chapter 4.3.6 --- Discussion --- p.104 / Chapter 4.4 --- ALTERATION OF FECAL EXCRETION BY DIETARY CLA --- p.105 / Chapter 4.4.1 --- Objective of The Present Study --- p.108 / Chapter 4.4.2 --- Materials and Methods --- p.109 / Chapter 4.4.2.1 --- Separation of Neutral and Acidic Sterols --- p.109 / Chapter 4.4.2.2 --- Neutral Sterol Analysis --- p.109 / Chapter 4.4.2.3 --- Acidic Sterol Analysis --- p.110 / Chapter 4.4.2.4 --- GLC Analysis of Neutral and Acidic Sterols --- p.110 / Chapter 4.4.3 --- Statistics --- p.113 / Chapter 4.4.4 --- Results --- p.114 / Chapter 4.4.4.1 --- Effect of CLA Supplementation on Fecal Output of Neutral Sterols --- p.114 / Chapter 4.4.4.2 --- Effect of CLA Supplementation on Fecal Output of Acidic Sterols --- p.114 / Chapter 4.4.5 --- Discussion --- p.118 / Chapter Chapter5 --- Conclusions --- p.123 / References --- p.126

Yeung Ming. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves 136-162). / Abstracts in English and Chinese. / THESIS COMMITTEE --- p.i / ACKNOWLEDGEMENTS --- p.ii / ABSTRACT (ENGLISH) --- p.iii~v / ABSTRACT (CHINESE) --- p.vi~vii / TABLE OF CONTENTS --- p.viii~xiii / LIST OF TABLES --- p.xiv~xv / LIST OF FIGURES --- p.xvi~xviii / LIST OF ABBREVIATIONS --- p.xix~xx / Chapter CHAPTER ONE: --- INTRODUCTION --- p.1 / Chapter 1.1 --- Different lipoproteins and their functions --- p.1 / Chapter 1.1.1 --- Chylomicrons --- p.4 / Chapter 1.1.2 --- VLDL --- p.4 / Chapter 1.1.3 --- LDL --- p.4 / Chapter 1.1.4 --- HDL --- p.5 / Chapter 1.2 --- Risk factors of coronary heart disease (CHD) --- p.5 / Chapter 1.2.1 --- Background information of CHD --- p.6 / Chapter 1.2.2 --- "Relationship between serum total cholesterol (TC), Low-density lipoprotein (LDL) cholesterol and CHD" --- p.7 / Chapter 1.2.3 --- High-density lipoprotein (HDL) cholesterol and CHD --- p.8 / Chapter 1.2.4 --- Triglyceride and CHD --- p.9 / Chapter 1.3 --- Cholesterol homeostasis --- p.10 / Chapter 1.3.1 --- Roles of HMG-CoA reductase in cholesterol biosynthesis --- p.13 / Chapter 1.3.2 --- Roles of cholesterol 7α-hydroxylase (CYP7A) in cholesterol catabolism…… --- p.15 / Chapter 1.3.3 --- Effects of Short-Chain Fatty Acid (SCFA) --- p.17 / Chapter 1.3.4 --- Related hormone --- p.18 / Chapter 1.4 --- Possible mechanisms of hypolipidemic agents --- p.19 / Chapter 1.4.1 --- Hypolipidemic functional foods --- p.20 / Chapter 1.4.2 --- Pharmacological drugs --- p.26 / Chapter 1.5 --- Edible and medicinal mushrooms --- p.28 / Chapter 1.5.1 --- General introduction --- p.28 / Chapter 1.5.2 --- Hypolipidemic agents from Fungi --- p.31 / Chapter 1.6 --- Animal model --- p.35 / Chapter 1.7 --- Objectives --- p.36 / Chapter CHAPTER TWO: --- MATERIALS AND METHODS --- p.37 / Chapter 2.1 --- Materials --- p.37 / Chapter 2.1.1 --- Mushroom samples and control --- p.37 / Chapter 2.1.1.1 --- Sample introduction --- p.37 / Chapter 2.1.1.2 --- Sample collection --- p.40 / Chapter 2.1.1.3 --- Sample preparation --- p.41 / Chapter 2.1.1.4 --- Moisture content --- p.45 / Chapter 2.1.2 --- Animal diets for different experiments --- p.45 / Chapter 2.1.2.1 --- Basal diet --- p.45 / Chapter 2.1.2.2 --- Diet for preliminary screening --- p.46 / Chapter 2.1.2.3 --- Diet for dosage experiment --- p.46 / Chapter 2.1.2.4 --- Diet for active ingredient experiments --- p.47 / Chapter 2.1.2.5 --- Diet for long-term feeding experiment --- p.47 / Chapter 2.1.3 --- Animal model --- p.49 / Chapter 2.2 --- Methods --- p.49 / Chapter 2.2.1 --- Nutritional components of mushroom samples --- p.49 / Chapter 2.2.1.1 --- Crude protein content (Kjeldahl method) --- p.49 / Chapter 2.2.1.2 --- Total dietary fiber content --- p.50 / Chapter 2.2.1.3 --- Crude lipid content --- p.52 / Chapter 2.2.1.4 --- Ash content --- p.53 / Chapter 2.2.1.5 --- Moisture content --- p.53 / Chapter 2.2.2 --- Animal handling experiments --- p.54 / Chapter 2.2.2.1 --- Feeding experiment standards --- p.54 / Chapter 2.2.2.1.1 --- Feeding experiments of preliminary screening test --- p.54 / Chapter 2.2.2.1.2 --- Feeding experiments of dosage test --- p.55 / Chapter 2.2.2.1.3 --- Feeding experiments of solvent extracts from Agrocybe aegerita (Brig) Sing (AA) --- p.56 / Chapter 2.2.2.1.3.1 --- Fractionation of ethanol & water soluble components of AA --- p.56 / Chapter 2.2.2.1.3.2 --- Feeding experiments of ethanol & water soluble components of AA --- p.57 / Chapter 2.2.2.1.4 --- Feeding experiment of long-term test --- p.58 / Chapter 2.2.2.2 --- Blood sample collection --- p.58 / Chapter 2.2.2.3 --- Serum preparation --- p.58 / Chapter 2.2.2.4 --- Liver sample preparation --- p.58 / Chapter 2.2.2.5 --- Fecal sample preparation --- p.59 / Chapter 2.2.3 --- Determination of serum lipid profiles --- p.59 / Chapter 2.2.3.1 --- Serum total cholesterol (TC) assay --- p.59 / Chapter 2.2.3.2 --- Serum triglyceride (TG) assay --- p.60 / Chapter 2.2.3.3 --- Serum high-density lipoprotein (HDL) cholesterol assay --- p.61 / Chapter 2.2.3.3.1 --- Separation of HDL fraction --- p.61 / Chapter 2.2.3.3.2 --- HDL cholesterol (HDL-c) determination --- p.61 / Chapter 2.2.4 --- Determination of liver lipid profiles --- p.62 / Chapter 2.2.4.1 --- Liver total cholesterol (TC) level determination --- p.62 / Chapter 2.2.4.2 --- Determination of liver total lipid (TL) level --- p.64 / Chapter 2.2.5 --- Quantitative determination of fecal neutral & acidic sterols --- p.64 / Chapter 2.2.5.1 --- Separation of fecal neutral & acidic sterols --- p.64 / Chapter 2.2.5.2 --- Derivatisation of fecal neutral sterols --- p.65 / Chapter 2.2.5.3 --- Derivatisation of fecal acidic sterols --- p.65 / Chapter 2.2.5.4 --- Gas chromatographic analysis of fecal neutral & acidic sterols --- p.66 / Chapter 2.2.6 --- Assays of liver key enzymes in cholesterol metabolism --- p.67 / Chapter 2.2.6.1 --- Preparation of hepatic microsome --- p.67 / Chapter 2.2.6.2 --- Assay of HMG-CoA reductase activity --- p.68 / Chapter 2.2.6.3 --- Assay of CYP7A activity --- p.69 / Chapter 2.3 --- Data statistics --- p.71 / Chapter CHAPTER THREE: --- RESULTS AND DISCUSSION --- p.72 / Chapter 3.1 --- Preliminary screening of eleven mushrooms for their hypolipidemic effect in hyperlipidemic S.D. rats --- p.72 / Chapter 3.1.1 --- Body weight and food intake --- p.73 / Chapter 3.1.2 --- Effect of mushroom supplementation on serum lipid profiles --- p.75 / Chapter 3.1.2.1. --- Effect of mushroom supplementation on serum TC levels --- p.75 / Chapter 3.1.2.2. --- Effect of mushroom supplementation on serum TG levels --- p.77 / Chapter 3.1.2.3. --- Effect of mushroom supplementation on serum HDL levels --- p.79 / Chapter 3.1.2.4 --- Discussion of serum lipid profiles of S.D. rats fed M.S. diets in mushroom screening experiments --- p.83 / Chapter 3.1.3 --- Effect and discussion of mushroom supplementation on hepatic lipid profiles --- p.84 / Chapter 3.1.4 --- Effect and discussion of mushroom supplementation on fecal neutral sterol excretion --- p.87 / Chapter 3.1.5 --- Summary (mushroom screening experiments) --- p.90 / Chapter 3.2 --- Hypolipidemic effect of Agrocybe aegerita (Brig.) Sing (AA) in a dose response study in hyperlipidemic S.D. rats --- p.91 / Chapter 3.2.1 --- Nutritional composition of AA mushroom --- p.91 / Chapter 3.2.2 --- Body weight and food intake --- p.91 / Chapter 3.2.3 --- Effect of three different dosages of AA mushroom supplementation on blood lipid profiles of S.D. rats --- p.93 / Chapter 3.2.3.1 --- Effect of different dosages of AA mushroom supplementation diets on serum TC level --- p.93 / Chapter 3.2.3.2 --- Effect of different dosages of AA mushroom supplementation diets on serum TG level --- p.93 / Chapter 3.2.3.3 --- Effect of different dosages of AA mushroom supplementation diets on serum HDL level --- p.95 / Chapter 3.2.3.4 --- Discussion of different dosages of AA mushroom supplementation diets on serum lipid profiles --- p.97 / Chapter 3.2.4 --- Effect and discussion of three different dosages of AA mushroom supplementation on hepatic lipid profiles --- p.98 / Chapter 3.2.5 --- Effect and discussion of three different dosages of AA mushroom supplementation on fecal neutral & acidic sterol excretion --- p.101 / Chapter 3.2.6 --- Summary (dose response study) --- p.105 / Chapter 3.3 --- Hypolipidemic effect of ethanol extract (E.E.) & water extract (W.E.) from AA in hyperlipidemic S.D. rats --- p.106 / Chapter 3.3.1 --- Extraction yield --- p.106 / Chapter 3.3.2 --- Body weight & food intake --- p.106 / Chapter 3.3.3 --- Effect of AA extract supplementation on serum lipid profiles --- p.107 / Chapter 3.3.3.1 --- Effect of AA extract supplementation on serum TC level --- p.107 / Chapter 3.3.3.2 --- Effect of AA extract supplementation on serum TG level --- p.108 / Chapter 3.3.3.3 --- Effect of AA extract supplementation on serum HDL level --- p.109 / Chapter 3.3.4 --- Effect of AA extract supplementation on hepatic lipid profiles --- p.111 / Chapter 3.3.5 --- Effect of AA extract supplementation on fecal neutral & acidic sterols excretion --- p.111 / Chapter 3.3.6 --- Discussion (active fraction extract study) --- p.113 / Chapter 3.4 --- Long-term evaluation of the hypolipidemic effect of AA supplementation in normolipic S.D. rats --- p.116 / Chapter 3.4.1 --- Body weight & food intake --- p.116 / Chapter 3.4.2 --- Effect of long term AA supplementation on serum lipid profiles --- p.117 / Chapter 3.4.2.1 --- Effect of long term AA supplementation on serum TC level --- p.117 / Chapter 3.4.2.2 --- Effect of long term AA supplementation on serum TG level --- p.118 / Chapter 3.4.2.3 --- Effect of long term AA supplementation on serum HDL level --- p.119 / Chapter 3.4.3 --- Effect of long term AA supplementation on hepatic lipid profiles --- p.119 / Chapter 3.4.4 --- Effect of long term AA supplementation on fecal neutral & acidic sterols excretion --- p.121 / Chapter 3.4.5 --- Effect of long term AA supplementation on hepatic key enzymes of cholesterol metabolism ´ؤ HMG-CoA reductase and CYP7A --- p.123 / Chapter 3.4.5.1 --- Quantitation of hepatic microsomal protein --- p.123 / Chapter 3.4.5.2 --- Effect of long term AA supplementation on HMG-CoA reductase activity in S.D. rats --- p.124 / Chapter 3.4.5.3 --- Effect of long term AA supplementation on CYP7A activity in S.D. rats --- p.124 / Chapter 3.4.7 --- Discussion (long-term study) --- p.126 / Chapter CHAPTER FOUR: --- CONCLUSION AND FUTURE PERSPECTIVES --- p.130 / References --- p.136

by Chan Ping Tim Timothy. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (leaves 129-141). / ACKNOWLEDGMENTS --- p.I / ABSTRACT --- p.II / LIST OF ABBREVIATIONS --- p.IV / TABLE OF CONTENTS --- p.VI / Chapter CHAPTER 1 --- GENERAL INTRODUCTION --- p.1 / Chapter 1.1 --- History of tea --- p.1 / Chapter 1.2 --- Botany and agriculture of tea --- p.1 / Chapter 1.3 --- Classification of tea --- p.2 / Chapter 1.4 --- Composition of tea --- p.4 / Chapter 1.5 --- Tea processing --- p.8 / Chapter 1.5.1 --- Manufacture of green tea --- p.8 / Chapter 1.5.2 --- Manufacture of black tea --- p.8 / Chapter 1.5.3 --- Manufacture of oolong tea --- p.10 / Chapter 1.6 --- Pharmacological effects of tea catechins --- p.13 / Chapter 1.6.1 --- Antioxidative activity --- p.13 / Chapter 1.6.2 --- Hypolipidemic activity --- p.14 / Chapter 1.6.3 --- Antimutagenic activity --- p.15 / Chapter 1.6.4 --- Anticarcinogenic activity --- p.15 / Chapter 1.6.5 --- Antibacterial activity --- p.16 / Chapter CHAPTER 2 --- ANTIOXIDATIVE ACTIVITIES OF TEA ETHANOL EXTRACTS AND GTC ON OXIDATION OF CANOLA OIL --- p.18 / Chapter 2.1 --- Introduction --- p.18 / Chapter 2.1.1 --- Lipid oxidation in food --- p.18 / Chapter 2.1.2 --- Phenolic antioxidants --- p.19 / Chapter 2.1.2.1 --- Major phenolic antioxidants used in food --- p.19 / Chapter 2.1.2.2 --- Mechanism of action of phenolic antioxidants --- p.20 / Chapter 2.1.2.3 --- BHA and its safety --- p.22 / Chapter 2.1.2.4 --- BHT and its safety --- p.24 / Chapter 2.1.3 --- Natural antioxidants --- p.24 / Chapter 2.2 --- Objectives --- p.26 / Chapter 2.3 --- Materials --- p.28 / Chapter 2.4 --- Methods --- p.28 / Chapter 2.4.1 --- GTC extraction --- p.28 / Chapter 2.4.2 --- "HPLC analysis of GTC," --- p.29 / Chapter 2.4.3 --- Isolation and purification of individual epicatechin isomers --- p.30 / Chapter 2.4.4 --- Ethanol extraction of tea --- p.30 / Chapter 2.4.5 --- Effect of tea ethanol extracts on oxygen consumption of canola --- p.31 / Chapter 2.4.6 --- Effect of GTC on oxygen consumption of canola oil --- p.32 / Chapter 2.4.7 --- Fatty acid analysis --- p.32 / Chapter 2.4.8 --- Thermal loss of BHT --- p.33 / Chapter 2.4.9 --- Thermal loss of GTC --- p.33 / Chapter 2.4.10 --- Statistics --- p.35 / Chapter 2.5 --- Results --- p.37 / Chapter 2.5.1 --- Antioxidative activities of tea ethanol extracts --- p.37 / Chapter 2.5.2 --- The yield and composition of GTC from jasmine tea --- p.51 / Chapter 2.5.3 --- Antioxidative activity of GTC --- p.55 / Chapter 2.5.4 --- Antioxidative activities of individual epicatechin isomers --- p.55 / Chapter 2.5.5 --- Thermal loss of GTC --- p.60 / Chapter 2.6 --- Discussion --- p.62 / Chapter 2.6.1 --- Contribution of catechins to the antioxidative effects of tea ethanol extracts --- p.62 / Chapter 2.6.2 --- Antioxidaitve activities of different types of teas --- p.62 / Chapter 2.6.3 --- Proposed mechanisms for the relative activity of epicatechin isomers --- p.63 / Chapter 2.6.4 --- Loss of BHT via volatilization --- p.66 / Chapter 2.6.5 --- Potential of tea catechins as food antioxidants --- p.67 / Chapter 2.6.5.1 --- Safety of GTC --- p.67 / Chapter 2.6.5.2 --- Solubility of GTC --- p.68 / Chapter 2.6.5.3 --- Effects of GTC on food quality --- p.68 / Chapter CHAPTER 3 --- INHIBITORY EFFECTS OF GTC AND EPICATECHIN ISOMERS ON IN VITRO CU2+-MEDIATED LDL OXIDATION --- p.70 / Chapter 3.1 --- Introduction --- p.70 / Chapter 3.1.1 --- Mechanisms of LDL oxidation --- p.71 / Chapter 3.1.1.1 --- Nature and sources of oxidants underlying LDL oxidation --- p.71 / Chapter 3.1.1.2 --- Structural changes of ox-LDL --- p.72 / Chapter 3.1.2 --- Biological effects of ox-LDL --- p.74 / Chapter 3.1.3 --- Antioxidants and atherosclerosis --- p.76 / Chapter 3.2 --- Objectives --- p.78 / Chapter 3.3 --- Materials and methods --- p.79 / Chapter 3.3.1 --- LDL isolation --- p.79 / Chapter 3.3.2 --- LDL oxidation --- p.79 / Chapter 3.3.3 --- Thiobarbituric acid-reactive substance (TBARS) assay --- p.80 / Chapter 3.3.4 --- Lipid analysis --- p.80 / Chapter 3.3.5 --- Statistics --- p.81 / Chapter 3.4 --- Results --- p.82 / Chapter 3.4.1 --- Protective effects of GTC against LDL oxidation --- p.82 / Chapter 3.4.2 --- Varying protective effects of individual epicatechin isomers --- p.82 / Chapter 3.4.3 --- Protective effects of GTC against oxidative degradation of PUFAs in LDL --- p.86 / Chapter 3.5 --- Discussion --- p.88 / Chapter 3.5.1 --- Tea catechins as anti-atherogenic agents --- p.88 / Chapter 3.5.2 --- Mechanisms of the protective effects of tea catechins against Cu2+-induced LDL oxidation --- p.88 / Chapter 3.5.3 --- Relative antioxidative activities of epicatchin isomers --- p.89 / Chapter 3.5.4 --- Absorption of tea catechins --- p.90 / Chapter 3.5.5 --- Pro-oxidant activities of tea catechins --- p.91 / Chapter CHAPTER 4 --- HYPOLIPIDEMIC ACTIVITY OF GTC --- p.93 / Chapter 4.1 --- Introduction --- p.93 / Chapter 4.1.1 --- High serum cholesterol as a risk factor of CHD --- p.93 / Chapter 4.1.2 --- Serum TG and CHD --- p.94 / Chapter 4.1.3 --- Hypolipidemic effect of tea --- p.95 / Chapter 4.1.4 --- Hamster as an animal model of cholesterol metabolism --- p.96 / Chapter 4.2 --- Objectives --- p.97 / Chapter 4.3 --- Materials and methods --- p.98 / Chapter 4.3.1 --- Animals --- p.98 / Chapter 4.3.2 --- Experiment 1 --- p.98 / Chapter 4.3.3 --- Experiment 2 --- p.100 / Chapter 4.3.4 --- Experiment 3 --- p.101 / Chapter 4.3.5 --- "Serum lipid, lipoprotein and apolipoprotein determinations" --- p.101 / Chapter 4.3.6 --- Lipid analysis of liver and carcass --- p.102 / Chapter 4.3.7 --- Analysis of fecal lipid content --- p.102 / Chapter 4.3.8 --- Determination of hepatic cholesterol content --- p.103 / Chapter 4.3.9 --- Assay of fatty acid synthase activity --- p.105 / Chapter 4.3.10 --- Statistics --- p.105 / Chapter 4.4 --- Results --- p.106 / Chapter 4.4.1 --- Growth and food intake --- p.106 / Chapter 4.4.2 --- Effects of different levels of dietary GTC on serum TG and cholesterol --- p.106 / Chapter 4.4.3 --- Time course study of the hypolipidemic effects of dietary GTC --- p.109 / Chapter 4.4.4 --- Effects of GTWE on serum lipid and apolipoprotein profiles --- p.113 / Chapter 4.4.5 --- "Effects of dietary GTC on hepatic TG, FFA and cholesterol contents" --- p.113 / Chapter 4.4.6 --- "Effects of dietary GTC on carcass TG, FFA and cholesterol contents" --- p.118 / Chapter 4.4.7 --- Effects of dietary GTC on fatty acid synthase activity --- p.118 / Chapter 4.4.8 --- Effects of dietary GTC on fecal lipids content --- p.118 / Chapter 4.5 --- Discussion --- p.120 / Chapter 4.5.1 --- Hypolipidemic effect of GTC --- p.120 / Chapter 4.5.2 --- Effects of GTC on serum apolipoproteins --- p.120 / Chapter 4.5.3 --- Implication of GTC intake in humans --- p.121 / Chapter 4.5.4 --- Mechanisms for the hypolipidemic activity of GTC --- p.122 / Chapter 4.5.5 --- Reduction in hepatic TG and FFA contents in GTC-fed hamsters --- p.123 / Chapter 4.5.6 --- Suppression of body lipid accumulation by dietary GTC --- p.124 / Chapter 4.5.7 --- Mechanisms for the hypocholesterolemic activity of GTC --- p.124 / Chapter CHAPTER 5 --- CONCLUSIONS --- p.126 / REFERENCES --- p.129

by Zhang Ze Sheng. / "October 2001." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (p. 157-174). / 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.

Charles University Faculty of Pharmacy in Hradec Králové Department of Pharmacology and Toxicology Student: Jan Juhász Supervisor: Prof. MUDr. Radomír Hrdina, CSc. Title of diploma thesis: Treatment of lower extremity peripheral artery disease The lower extremities ischemia is a disease caused most often by atherosclerosis during which the lumen in lower limb arteries becomes narrow. Its prevalence is increasing, especially in the developed countries. The disease can be asymptomatic and symptomatic. The symptoms are very unpleasant and decrease patient's quality of life. Advanced stages of the disease may be life threatening. Therefore, it is vital to timely and correctly diagnose the illness. During the therapy, it is possible to use pharmacological as well as non-pharmacological procedures, and, preferably, a combination of the two types of treatment. The pharmacotherapy can be divided into several parts. The prevention of atherosclerotic complications makes use of preventive measures and antiplatelet therapy to reduce the cardiovascular risk. The symptoms therapy focuses on improving patients' quality of life by prescribing the vasoactive medications cilostazol, naftidrofuryl or pentoxifylin. The critical limb ischemia therapy uses prostaglandin analogues alprostadil, iloprost, limaprost or...