Background: Cardiovascular disease is the leading cause of mortality and morbidity in the world and has something to do with daily diet. The polyphenol is the most abundant compound in daily diet, including grape. The red wine was rich in polyphenol because of composing much grape. Early study has already confirmed the “French Paradox” in cardiovascular protection power, which shed light on the dietary modulation on disease. Objective: The main objective of the study was to evaluate the effect of products containing polyphenol such as red wine extract, grape juice and grape extract tablets or powder on cardiovascular disease risk factors. It mainly examined relationship between polyphenol and serum lipid in addition to blood pressure. Methods: Studies working on effects of grape extract products on cardiovascular disease were searched from electronic resources MEDLINE and EMBASE. Nine clinical controlled trials were identified through PubMed and Ovid. CONSORT guideline and Jadad Score were used to appraise the quality of trials. Weighing two assessment guidelines, a total of three studies were in good quality, one was in bad quality while the rest four were fair to middle. Results: The changes before and after intervention on serum lipid and blood pressure were contradictory. Some studies found polyphenol was statistically significant protective factors, while some did not find it siginificant but still showed a protective effect. One study found polyohenol had no effect on cardiovascular disease risk factors. Conclusion: The prevention of polyphenol was not consistent in nine trials and there is no sufficient and strong evidence supporting its cardiovascular protection effect given that the study design of each trial differed. It was not recommeded to use grape polyphenol as cardiovascular protect products. There were limitations and weakness of current study on the association of polyphenol and cardiovascular disease. Further research on this topic is required, both in vivo and in vitro. / published_or_final_version / Public Health / Master / Master of Public Health

published_or_final_version / Anatomy / Doctoral / Doctor of Philosophy

abstract / Medicine / Master / Master of Philosophy

published_or_final_version / Anatomy / Doctoral / Doctor of Philosophy

Thesis (MTech (Consumer Science: Food and Nutrition))--Cape Peninsula University of Technology, 2016. / Background: The different types and forms of rooibos and the ways in which it is prepared and flavoured for consumption influences its total polyphenol content and total antioxidant capacity (TAC) and hence depends on its consumer practices. Design: Phase 1 of the study entailed the selection and preparation of different rooibos types and forms; rooibos brewed for different times; and with different household and commercially added flavourings to determine the total polyphenol content, TAC, flavonol and flavanol content; and subsequent identification of the optimal cup of rooibos based on the first two biochemical parameters. For Phase 2 a questionnaire was used to obtain information on the profile of the adult rooibos herbal tea consumer, as well as of those consuming the optimal cup of rooibos. Results: The following prepared rooibos samples delivered the higher biochemical parameter content: green / unfermented (type representative); green / unfermented leaves and powdered extract (form representatives); that brewed for 10 minutes or longer; and those with added honey. The optimal cup of rooibos was identified as the one brewed for 10 minutes or longer. The older respondents and those with a lower level of education consumed a higher daily amount of rooibos (p < 0.05) and those who brewed rooibos in a teapot consumed the optimal cup (p < 0.05). However, very few respondents consumed the advised number of cups per day (< 1%) and the identified optimal cup (15.9%). Conclusions: Rooibos consumers in this study did not consume it in sufficient amounts and did not brew it for long enough to fully gain from its attributed health benefits.

Lam, Cheuk Kai. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 148-173). / Abstracts in English and Chinese. / ACKNOWLEDGEMENTS --- p.i / ABSTRACT --- p.ii / LIST OF ABBREVIATIONS --- p.vi / TABLE OF CONTENTS --- p.x / Chapter CHAPTER 1 --- GENERAL INTRODUCTION / Chapter 1.1 --- Introduction to Cholesterol and Its Related Diseases --- p.1 / Chapter 1.1.1 --- Chemistry of cholesterol --- p.1 / Chapter 1.1.2 --- Physiological importance of cholesterol --- p.1 / Chapter 1.1.3 --- Pathological effects of cholesterol --- p.3 / Chapter 1.1.3.1 --- Mechanism of atherosclerosis --- p.3 / Chapter 1.2 --- Cholesterol Homeostasis --- p.6 / Chapter 1.2.1 --- Liver as the main organ for cholesterol metabolism --- p.6 / Chapter 1.2.2 --- Regulatory sites of cholesterol metabolism --- p.6 / Chapter 1.2.2.1 --- Regulation of cholesterol absorption by acyl coenzyme A: cholesterol acyltransferase (ACAT) --- p.6 / Chapter 1.2.2.2 --- Sterol regulatory element-binding protein 2 (SREBP-2) as a transcription factor for 3 -hydroxy-3 -methylglutaryl coenzyme A reductase (HMGR) and low-density lipoprotein receptor (LDLR) --- p.10 / Chapter 1.2.2.3 --- Roles ofLDLR --- p.11 / Chapter 1.2.2.4 --- Rate limiting role of HMGR in cholesterol de novo synthesis --- p.14 / Chapter 1.2.2.5 --- Roles of liver-X-receptor-a (LXR-a) in cholesterol catabolism --- p.16 / Chapter 1.2.2.6 --- Roles of CYP7A1 in catabolism of cholesterol into bile acids --- p.19 / Chapter 1.2.2.7 --- Roles of cholesterol ester transfer protein (CETP) in maintaining cholesterol distribution in blood --- p.22 / Chapter CHAPTER 2 --- EFFECT OF OCTADECAENOIC ACIDS ON BLOOD CHOLESTEROL IN HAMSTERS / Chapter 2.1 --- Introduction --- p.25 / Chapter 2.1.1 --- Effects of polyunsaturated fatty acids (PUFAs) on blood cholesterol --- p.25 / Chapter 2.1.2 --- Differential effects of 18-C PUFAs on lowering blood cholesterol in vivo --- p.25 / Chapter 2.1.3 --- "Structures, metabolism and conjugation of octadecaenoic acids (ODA)" --- p.26 / Chapter 2.1.4 --- Objectives --- p.26 / Chapter 2.2 --- Experiment 1 --- p.28 / Chapter 2.2.1 --- Materials and methods --- p.28 / Chapter 2.2.1.1 --- Experimental fatty acids --- p.28 / Chapter 2.2.1.1.1 --- Isolation of LN from flaxseed --- p.28 / Chapter 2.2.1.1.2 --- Isolation of CLN from tung seed --- p.28 / Chapter 2.2.1.2 --- Animals --- p.29 / Chapter 2.2.1.3 --- Diets --- p.30 / Chapter 2.2.1.4 --- Plasma lipid measurements --- p.30 / Chapter 2.2.1.5 --- Plasma CETP activity measurement --- p.30 / Chapter 2.2.1.6 --- "Measurement of liver SREBP-2, LDLR, HMGR and CYP7A1 protein abundance by Western blotting" --- p.34 / Chapter 2.2.1.7 --- "Measurement of hepatic SREBP-2, LDLR, HMGR, LXR, CYP7A1, CETP, SR-B1 and LCAT mRNA by real time PCR" --- p.35 / Chapter 2.2.1.7.1 --- Extraction of mRNA --- p.35 / Chapter 2.2.1.1.2 --- Complementary DNA synthesis --- p.36 / Chapter 2.2.1.7.3 --- Real-time polymerase chain reaction (PCR) anaylsis --- p.36 / Chapter 2.2.1.8 --- Determination of cholesterol in liver --- p.37 / Chapter 2.2.1.9 --- Determination of fecal neutral and acidic sterols --- p.38 / Chapter 2.2.1.9.1 --- Determination of fecal neutral sterols --- p.39 / Chapter 2.2.1.9.2 --- Determination of fecal acidic sterols --- p.41 / Chapter 2.2.1.10 --- Statistics --- p.43 / Chapter 2.2.2 --- Results --- p.44 / Chapter 2.2.2.1 --- Growth and food intake --- p.44 / Chapter 2.2.2.2 --- Organ weights --- p.44 / Chapter 2.2.2.3 --- "Effects of ODA on serum TC, TG and HDL-C" --- p.44 / Chapter 2.2.2.4 --- Effect of ODA on liver cholesterol --- p.48 / Chapter 2.2.2.5 --- Effect of ODA on fecal neutral sterol output --- p.48 / Chapter 2.2.2.6 --- Effect of ODA on fecal acidic sterol output --- p.48 / Chapter 2.2.2.7 --- Effect of ODA on cholesterol balance in hamsters --- p.52 / Chapter 2.2.2.8 --- Effect of ODA on plasma CETP activity --- p.52 / Chapter 2.2.2.9 --- Correlation between blood TC and liver cholesterol --- p.52 / Chapter 2.2.2.10 --- Correlation between blood HDL-C and liver cholesterol --- p.52 / Chapter 2.2.2.11 --- Correlation between blood nHDL/HDL ratio and liver cholesterol --- p.52 / Chapter 2.2.2.12 --- Effect ofODA on liver SREBP-2 immunoreactive mass --- p.58 / Chapter 2.2.2.13 --- Effect of ODA on liver LDLR immunoreactive mass --- p.58 / Chapter 2.2.2.14 --- Effect of ODA on liver HMGR immunoreactive mass --- p.58 / Chapter 2.2.2.15 --- Effect of ODA on liver LXR immunoreactive mass --- p.58 / Chapter 2.2.2.16 --- Effect of ODA on liver CYP7A1 immunoreactive mass --- p.63 / Chapter 2.2.2.17 --- Effects ofODA on hepatic CETP mRNA --- p.65 / Chapter 2.2.2.18 --- Effects of ODA on hepatic LDLR mRNA --- p.65 / Chapter 2.2.2.19 --- Effects of ODA on hepatic LXR mRNA --- p.65 / Chapter 2.2.2.20 --- Effects of ODA on hepatic CYP7A1 mRNA --- p.65 / Chapter 2.3 --- Experiment 2 --- p.70 / Chapter 2.3.1 --- Materials and Methods --- p.70 / Chapter 2.3.1.1 --- Experimental diets --- p.70 / Chapter 2.3.1.2 --- Animals --- p.70 / Chapter 2.3.1.3 --- Intestinal acyl coenzyme A: cholesterol acyltransferase (ACAT) activity measurement --- p.70 / Chapter 2.3.1.3.1 --- Preparation of intestinal microsome --- p.71 / Chapter 2.3.1.3.2 --- ACAT activity assay --- p.71 / Chapter 2.3.2 --- Results --- p.73 / Chapter 2.3.2.1 --- Growth and food intake --- p.73 / Chapter 2.3.2.2 --- Organ weights --- p.73 / Chapter 2.3.2.3 --- "Effect of ODA on serum TC, TG and HDL-C" --- p.73 / Chapter 2.3.2.4 --- Effect of ODA feeding on fecal neutral sterol content --- p.77 / Chapter 2.3.2.5 --- Effect of ODA feeding on fecal acidic sterol content --- p.77 / Chapter 2.3.2.6 --- Effect of ODA feeding on intestinal acyl coenzyme A: acyl cholesterol transferase (ACAT) activity --- p.77 / Chapter 2.4 --- Discussion --- p.81 / Chapter CHAPTER 3 --- EFFECT OF OCTADECAENOIC ACIDS ON CHOLESTEROL-REGULATING GENES IN HepG2 / Chapter 3.1 --- Introduction --- p.86 / Chapter 3.1.1 --- HepG2 as a model of cholesterol regulation --- p.86 / Chapter 3.1.2 --- Effect of polyunsaturated fatty acids (PUFAs) on cholesterol regulating genes in cultured cells --- p.87 / Chapter 3.1.3 --- Objectives --- p.89 / Chapter 3.2 --- Materials and Methods --- p.90 / Chapter 3.2.1 --- Cell culture --- p.90 / Chapter 3.2.2 --- "Measurement of SREBP-2, LDLR, HMGR and CYP7A1 protein abundance by Western blotting" --- p.92 / Chapter 3.2.3 --- "Measurement of cellular SREBP-2, LDLR, HMGR, LXR, CYP7A1 and CETP mRNA by real time PCR" --- p.93 / Chapter 3.2.4 --- Statistics --- p.93 / Chapter 3.3 --- Results --- p.95 / Chapter 3.3.1 --- Effect of ODA on HepG2 SREBP-2 immunoreactive mass --- p.95 / Chapter 3.3.2 --- Effect of ODA on HepG2 HMGR immunoreactive mass --- p.95 / Chapter 3.3.3 --- Effect of ODA on HepG2 LDLR immunoreactive mass --- p.95 / Chapter 3.3.4 --- Effect of ODA on HepG2 LXR immunoreactive mass --- p.95 / Chapter 3.3.5 --- Effect of ODA on HepG2 CYP7A1 immunoreactive mass --- p.96 / Chapter 3.3.6 --- Effect of ODA supplementation on HepG2 SREBP-2 mRNA expression --- p.102 / Chapter 3.3.7 --- Effect of ODA supplementation on HepG2 SREBP-2 mRNA expression --- p.102 / Chapter 3.3.8 --- Effect of ODA supplementation on HepG2 LDLR mRNA expression --- p.102 / Chapter 3.3.9 --- Effect of ODA supplementation on HepG2 LXR mRNA expression --- p.106 / Chapter 3.3.10 --- Effect of ODA supplementation on HepG2 CYP7A1 mRNA expression --- p.106 / Chapter 3.3.11 --- Effect of ODA supplementation on HepG2 CETP mRNA expression --- p.106 / Chapter 3.4 --- Discussion --- p.110 / Chapter CHAPTER 4 --- EFFECT OF APPLE POLYPHENOLS ON BLOOD CHOLESTEROL IN HAMSTERS / Chapter 4.1 --- Introduction --- p.114 / Chapter 4.1.1 --- Apple is a commonly consumed fruit worldwide --- p.114 / Chapter 4.1.2 --- Potential health effects of apples --- p.114 / Chapter 4.1.3 --- Abundance of polyphenols in apple --- p.115 / Chapter 4.1.4 --- Fuji variety of apple --- p.116 / Chapter 4.1.5 --- Objectives --- p.116 / Chapter 4.2 --- Materials and Methods --- p.118 / Chapter 4.2.1 --- Isolation of AP --- p.118 / Chapter 4.2.2 --- Characterization of AP extract --- p.118 / Chapter 4.2.3 --- Effect of AP on CETP activity in vitro --- p.118 / Chapter 4.2.4 --- Effect of AP on blood cholesterol in hamsters --- p.119 / Chapter 4.2.4.1 --- Animals --- p.119 / Chapter 4.2.4.2 --- Diets --- p.120 / Chapter 4.2.4.3 --- Plasma lipids measurement --- p.121 / Chapter 4.2.4.4 --- Plasma CETP activity measurement and immunoreactive mass by Western blotting --- p.123 / Chapter 4.2.4.5 --- "Measurement of liver SREBP-2, LDL-R, HMG-R and CYP7A1 protein abundance by Western blotting" --- p.124 / Chapter 4.2.4.6 --- Statistics --- p.124 / Chapter 4.3 --- Results --- p.125 / Chapter 4.3.1 --- Polyphenol content in AP --- p.125 / Chapter 4.3.2 --- Effect of AP on CETP activity in vitro --- p.125 / Chapter 4.3.3 --- Growth and food intake --- p.128 / Chapter 4.3.4 --- Organ weights --- p.128 / Chapter 4.3.5 --- Effect of AP supplementation on the plasma lipid profile of hamsters --- p.131 / Chapter 4.3.6 --- Effect of AP feeding on plasma CETP activity of the hamsters --- p.131 / Chapter 4.3.7 --- Effect of AP on plasma CETP immunoreactive mass --- p.134 / Chapter 4.3.8 --- Effect of AP on liver SREBP-2 immunoreactive mass --- p.134 / Chapter 4.3.9 --- Effect of AP on liver LDLR immunoreactive mass --- p.134 / Chapter 4.3.10 --- Effect of AP on liver HMGR immunoreactive mass --- p.134 / Chapter 4.3.11 --- Effect of AP on liver CYP7A1 immunoreactive mass --- p.134 / Chapter 4.3.12 --- Effect of AP on liver cholesterol level --- p.140 / Chapter 4.4 --- Discussion --- p.142 / Chapter CHAPTER 5 --- CONCLUSION --- p.145 / REFERENCES --- p.148