by Lam Heung-wah, Angora. / Thesis (M. Phil.)--Chinese University of Hong Kong, 1992. / Includes bibliographical references (leaves 124-131). / ACKNOWLEDGEMENTS --- p.iv / ABSTRACT --- p.v / LIST OF ABBREVIATIONS --- p.vii / LIST OF TABLES --- p.viii / LIST OF FIGURES --- p.ix / INTRODUCTION --- p.1 / LITERATURE REVIEW --- p.4 / Chapter A. --- Some Aspects of Cardiovascular Physiology and Pharmacology --- p.4 / Chapter I. --- Fundamental Principles Governing regulation of Arterial Pressure --- p.4 / Chapter II. --- Hypertension --- p.12 / Chapter III. --- Antihypertensive Substances --- p.16 / Chapter B. --- Mushrooms and Their Medicinal Values --- p.29 / Chapter I. --- "The Straw Mushroom, V. volvacea" --- p.29 / Chapter II. --- "Mushrooms, Blood Pressure, and Related Changes" --- p.32 / MATERIALS AND METHODS --- p.39 / Chapter A. --- Basic Preparative Procedures --- p.39 / Chapter I. --- Preparation of Straw Mushroom Extract (SME) --- p.39 / Chapter II. --- Purification of SME by Dialysis --- p.40 / Chapter III. --- Preparation for In vivo Blood Pressure Measurement in Rats --- p.40 / Chapter IV. --- preparation of Right Atrium for In vitro Studies --- p.41 / Chapter V. --- Preparation of Artery Strip for In vitro Studies --- p.42 / Chapter B. --- Experiments Done --- p.43 / Chapter Experiment 1. --- Toxicity of SME --- p.43 / Chapter Experiment 2. --- Hypotensive Effect of SME and Dialyzed Samples --- p.44 / Chapter Experiment 3. --- Pharmacological Antagonist Studies --- p.45 / Chapter Experiment 4. --- Effect of Autonomic Ganglion Blocker and Alpha Blocker on Hypotensive Changes Induced by SME --- p.47 / Chapter Experiment 5. --- Study on Renin-Angiotensin and Kinin Systems --- p.48 / Chapter Experiment 6. --- Urinary and Sodium Excretion in Water-loaded Rats --- p.48 / Chapter Experiment 7. --- Chronotropic and Inotropic Studies on Isolated Right Atria --- p.49 / Chapter Experiment 8. --- Contractile Responses of SME & Its Dialyzed Samples on Rat Tail Artery Strips --- p.50 / Chapter Experiment 9. --- Effect of Adrenergic Blockers in SME Preconstricted Strips --- p.51 / Chapter Experiment 10. --- Acute Oral Effect of DUL8000 and DLL8000 from SME on Blood Pressure --- p.51 / Chapter Experiment 11. --- "Chronic Oral Effect of SME on Blood Pressure, Total Free Cholesterol and Triglyceride Levels" --- p.52 / Chapter C. --- Statistics --- p.55 / RESULTS --- p.56 / Chapter A. --- Toxicity of Straw Mushroom Extract (SME) --- p.56 / Chapter B. --- Effects of SME in Normotensive Rats --- p.56 / Chapter I. --- Blood Pressure Changes --- p.56 / Chapter II. --- Pharmacological Antagonists Studies --- p.58 / Chapter III. --- Converting Enzyme Activity --- p.60 / Chapter IV. --- Urinary and Sodium Excretion --- p.60 / Chapter V. --- In vitro Arterial and Cardiac Effects --- p.61 / Chapter C. --- Cardiovascular Effects of Dialyzed Samples of SME (Molecular Mass cutoffl2000) in Spontaneously Hypertensive Rats (SHR) and Normotensive Rats --- p.61 / Chapter I. --- Blood Pressure Changes --- p.61 / Chapter II. --- In vitro Arterial and Cardiac Effects --- p.62 / Chapter D. --- Cardiovascular Effects of Dialyzed Samples (DUL8000 and DLL8000) in Spontaneously Hypertensive Rats (SHR) and Normotensive Rats --- p.63 / Chapter I. --- Blood Pressure Changes --- p.63 / Chapter II. --- In vitro Arterial and Cardiac Effects --- p.65 / Chapter E. --- The Acute Oral Effect of SME on Blood Pressure --- p.68 / Chapter F. --- "Chronic Dietary Effect of SME on Blood Pressure, Total Free Serum Cholesterol and Triglyceride Levels" --- p.68 / DISCUSSION --- p.109 / Chapter A. --- The Hypotensive Effect of SME --- p.109 / Chapter B. --- The Hypotensive Action of SME: Mechanism of Action --- p.110 / Chapter C. --- The Cardiovascular Active Fractions in SME --- p.113 / Chapter D. --- "The Cardiovascular Effect of DUL8000 and DLL8000 in Rats with Reference to Age, Sex and Strains" --- p.115 / Chapter E. --- The Oral Effect of SME on Blood Pressure and on Serum Cholesterol and Triglyceride Levels --- p.118 / SUMMARY --- p.121 / REFERENCES --- p.124 / APPENDIXES --- p.132

by Fung Yin Lee, Annie. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 181-189). / ABSTRACT --- p.i / LIST OF ABBREVIATIONS --- p.iv / ACKNOWLEDGEMENT --- p.v / TABLE OF CONTENTS --- p.vi / LIST OF FIGURES --- p.ix / INTRODUCTION --- p.1 / LITERATURE REVIEW --- p.4 / Chapter I. --- A. Arterial pressure --- p.4 / Chapter B. --- Regulation of arterial pressure --- p.7 / Chapter II. --- Hypertension --- p.14 / Chapter III. --- Treatment of hypertension --- p.29 / Chapter IV. --- Plants and their effects on blood pressure --- p.48 / Chapter V. --- Characteristics of the three plants being studied --- p.50 / MATERIALS AND METHODS --- p.55 / Chapter A. --- Preparative procedures --- p.55 / Chapter 1. --- Preparation of plant extracts --- p.55 / Chapter 2. --- Animal preparation for invivo blood pressure measurement --- p.56 / Chapter 3. --- Preparation of right atria for in vitro studies --- p.56 / Chapter 4. --- Preparation of artery strips for in vitro studies --- p.57 / Chapter 5. --- Preparation for diuretic studies --- p.58 / Chapter B. --- Experiments done --- p.60 / Chapter 1. --- Cumulative dose response of individual plant extract --- p.60 / Chapter 2. --- Combination of plant extracts --- p.60 / Chapter 3. --- Pharmacological antagonists studies --- p.64 / Chapter a. --- Autonomic ganglion transmission --- p.64 / Chapter b. --- Alpha adrenergic activity --- p.64 / Chapter c. --- Beta adrenergic activity --- p.65 / Chapter d. --- Cholinergic activity --- p.65 / Chapter e. --- Histaminergic activity --- p.65 / Chapter f. --- Serotoninergic activity --- p.65 / Chapter 4. --- Urinary and sodium excretionin water loaded rats --- p.66 / Chapter 5. --- Studies on chronotropic and inotropic effects on isolated right atrium --- p.66 / Chapter a. --- Effect of individual plant extract --- p.66 / Chapter b. --- Effect of combination of plant extracts --- p.66 / Chapter 6. --- Effect of plant extract on contractile responses of rat tail artery strips --- p.70 / Chapter a. --- Effect of individual plant extract --- p.70 / Chapter b. --- Effect of combination of plant extracts --- p.70 / Chapter 7. --- Effect of acute oral feeding of plant extracts on blood pressure of rats --- p.71 / Chapter C. --- Statistics --- p.71 / RESULTS / Chapter A. --- Preparation of plant extracts --- p.72 / Chapter B. --- Effect of plant extracts on blood pressure changes --- p.72 / Chapter 1. --- Individual plant extract --- p.72 / Chapter 2. --- Combination of two plant extracts --- p.73 / Chapter 3. --- Combination of three plant extracts --- p.76 / Chapter C. --- Pharmacological antagonist studies --- p.79 / Chapter 1. --- Autonomic ganglion transmission --- p.79 / Chapter 2. --- Alpha adrenergic activity --- p.79 / Chapter 3. --- Beta adrenergic activity --- p.81 / Chapter 4. --- Cholinergic activity --- p.82 / Chapter 5. --- Histaminergic activity --- p.83 / Chapter 6. --- Serotoninergic activity --- p.84 / Chapter D. --- Urinary and sodium excretion in water loaded rats --- p.85 / Chapter E. --- Chronotropic and inotropic studies of isolated right atrium --- p.88 / Chapter 1. --- Effect of individual plant extract --- p.88 / Chapter 2. --- Effect of combination of plant extracts --- p.89 / Chapter F. --- Effect of plant extracts on contractile responses of rat tail artery strips --- p.101 / Chapter G. --- Effect of acute oral feeding of plant extracts on MAP of rats --- p.102 / DISCUSSION --- p.156 / Chapter A. --- Comment on preparation of plant extracts --- p.156 / Chapter B. --- The hypotensive effects of the plant extracts --- p.157 / Chapter C. --- The mechanism of action --- p.159 / Chapter D. --- The renal effect of plant extracts --- p.161 / Chapter E. --- The interaction of the hypotensive effect of plant extracts --- p.164 / Chapter F. --- In vitro studies --- p.167 / Chapter G. --- The oral effect of the plant extracts --- p.174 / SUMMARY --- p.176 / CONCLUSION --- p.179 / REFERENCES --- p.181 / APPENDIX --- p.190 / "Appendix I To study the hypotensive effects of trypsin treated green bean, rue and kelp" --- p.191 / "Appendix II To study the hypotensive effects of ether treated green bean, rue and kelp" --- p.194

Leung Lai-Kin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves 110-113). / Abstracts in English and Chinese. / Abstract English --- p.i / Chinese --- p.iii / Acknowledgments --- p.v / Table of contents --- p.vi / List of Tables --- p.ix / List of Figures --- p.x / List of Abbreviations --- p.xiii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter Chapter 2 --- Establishment of compound formulation --- p.4 / Chapter 2.1 --- Formulation research --- p.4 / Chapter 2.2 --- Aqueous extract preparation --- p.6 / Chapter 2.2.1 --- Materials and Methods --- p.6 / Chapter 2.2.2 --- Results --- p.7 / Chapter 2.2.3 --- Discussion --- p.9 / Chapter 2.3 --- Preliminary test --- p.10 / Chapter 2.3.1 --- Materials and Methods --- p.10 / Chapter 2.3.2 --- Results --- p.12 / Chapter 2.3.3 --- Discussion --- p.14 / Chapter Chapter 3 --- Quality Control --- p.15 / Chapter 3.1 --- HPLC standardization --- p.16 / Chapter 3.2 --- Materials and Methods --- p.19 / Chapter 3.3 --- Results --- p.20 / Chapter 3.4 --- Discussion --- p.28 / Chapter Chapter 4 --- Antioxidant study --- p.29 / Chapter 4.1 --- Red blood cell hemolysis model --- p.30 / Chapter 4.1.1 --- Materials and Methods --- p.30 / Chapter 4.1.2 --- Results --- p.30 / Chapter 4.1.3 --- Discussion --- p.32 / Chapter 4.2 --- Ischemia-Reperfusion on Langendorff --- p.33 / Chapter 4.2.1 --- Materials and Methods --- p.34 / Chapter 4.2.2 --- Results --- p.37 / Chapter 4.2.3 --- Discussion --- p.60 / Chapter Chapter 5 --- Vasodilation study --- p.61 / Chapter 5.1 --- Vasodilation in organ bath --- p.63 / Chapter 5.1.1 --- Materials and Methods --- p.63 / Chapter 5.1.2 --- Results --- p.65 / Chapter 5.1.3 --- Discussion --- p.79 / Chapter 5.2 --- Endothelium dependent vasodilation --- p.80 / Chapter 5.2.1 --- Materials and Methods --- p.80 / Chapter 5.2.2 --- Results --- p.83 / Chapter 5.2.3 --- Discussion --- p.95 / Chapter Chapter 6 --- Anti-platelet study --- p.96 / Chapter 6.1 --- CFU-MK plasma clot colony assay --- p.97 / Chapter 6.2 --- Materials and Methods --- p.97 / Chapter 6.3 --- Results --- p.100 / Chapter 6.4 --- Discussion --- p.103 / Chapter Chapter 7 --- Discussions and prospects --- p.104 / Chapter 7.1 --- Discussions --- p.104 / Chapter 7.2 --- Prospects --- p.107 / Chapter 7.2.1 --- TCM capsule with GMP --- p.107 / Chapter 7.2.2 --- Clinical Trial of the capsule --- p.109 / References --- p.110

丹參和葛根為我國民間常用的傳統藥材, 常用於心血管疾病的治療。本試驗主要研究丹參葛根複方(DG, 7:3)對大鼠基底動脈的舒張作用 及腦保護作用。 / 上述所有藥物對U46619預收縮的基底動脈環呈現濃度依賴性的舒張作用。一氧化氮合酶抑制劑L-NAME以及鳥苷酸環化酶抑制劑ODG部分抑制葛根素的舒張作用。在另一組去內皮試驗中, 腺苷酸環化酶抑制劑SQ22536, 鳥苷酸環化酶抑制劑ODG, 大電導鈣離子依賴型鉀通道抑制劑Iberiotoxin以及電壓門控型鉀通道抑制劑4-AP對所有藥物的舒張作用沒有影響。然而， ATP型鉀通道抑制劑格列本脲能夠抑制丹參葛根複方，丹參，葛根，丹參素，葛根素，大豆苷以及大豆苷元的最大舒張反應。內向整流型鉀通道抑制劑氯化鋇則降低丹參酚酸B和大豆苷元的最大反應值。非選擇性鉀通道抑制劑乙基氯化銨以及所有鉀通道抑制劑的混合物顯著抑制上述所有藥物的舒張作用。除了葛根素之外，所有的藥物動度依賴性的抑制氯化鈣所引起的血管收縮。 / 體內研究發現大鼠經歷10分鐘雙側頸總動脈夾閉合並低血壓，及24小時的複灌後，與假手術組動物相比，腦血流量顯著降低，氧化性損傷明顯可見。連續7天口服丹參葛根複方（0.3g/kg 和 3g/kg）, 丹參 (3g/kg)，或者葛根 (3g/kg)對血壓沒有影響。但是，高劑量的丹參葛根複方 (3g/kg) 能夠提高超氧化物歧化酶和過氧化氫酶的活性，抑制丙二醛和一氧化氮的產生。3g/kg的葛根可以提高超氧化物歧化酶的活性，3g/kg的丹參則能抑制一氧化氮的產生。在大鼠中動脈阻塞模型中，連續7天口服丹參葛根複方（3g/kg）能明顯降低腦部的梗死率，同時改善大鼠的神經行為學。 / 總體來說，研究發現丹參葛根複方，丹參，葛根，丹參酚酸B，大豆苷以及大豆苷元的血管舒張作用是通過開平滑肌細胞的通鉀離子通道以及抑制鈣離子內流而實現的。然而葛根素的血管舒張作用是內皮依賴性的，通過產生一氧化氮，開放平滑肌細胞的鉀離子通道而實現的。丹參葛根複方能起到一定的腦保護作用。總而言之，研究表明上述藥物可能會對阻塞性腦血管病的人群有益處。 / Danshen and gegen are used in traditional Chinese medicine for the treatment of cardiovascular diseases. In this study, the relaxant actions of a danshen and gegen formulation (DG; ratio 7:3) and its constituents were investigated on rat-isolated cerebral basilar artery. In addition, the neuroprotective effect of DG was explored in rats subjected to global and focal ischaemia. / DG and all its constituents produced concentration-dependent relaxation of the artery rings precontracted by U46619. Removal of the endothelium had no effect on their vasodilator actions except the maximum response (I[subscript max]) to puerarin was inhibited by 42%. The nitric oxide synthase (NOS) inhibitor L-NAME and guanylyl cyclase (GC) inhibitor ODQ but not the cyclo-oxygenase (COX) inhibitor flurbiprofen produced partial inhibition on the puerarin-induced effect. In a set of endothelium-denuded artery rings, adenylyl cyclase (AC) inhibitor SQ22536, GC inhibitor ODQ, KV channel inhibitor 4-aminopyridine (4-AP) and BK[subscript Ca) channel inhibitor iberiotoxin had no influence on their vasodilator actions. However, pretreatment with K[subscript ATP] channel inhibitor glibenclamide reduced Imax to DG, danshen, gegen, danshensu, puerarin, daidzein and daidzin. K[subscript IR] inhibitor barium chloride (BaCl₂) reduced II[subscript max] to salvianolic acid B and daidzein. The non-selective K⁺ channel inhibitor tetraethylammonium (TEA), or a combination of all the K⁺ channel inhibitors produced significant partial inhibitions on all the agents’ actions. Electrophysiological studies on smooth muscle cells isolated from rat basilar artery also confirmed that DG, danshen, gegen danshensu, puerarin, daidzein and daidzin elevated K[subscript ATP] currents. In addition, DG and all its constituents, except puerarin, produced concentration-dependent inhibition on CaCl₂-induced vasoconstrictions. These findings were confirmed by con-focal microscopy studies. / In vivo study on a rat model of global ischaemia showed that challenging the rats with 10 min bilateral common carotid artery occlusion combined with hypotension, and followed by 24 h reperfusion produced significant decrease in cerebral blood flow and oxidative damage compared to sham-operated animals. Administration of DG (0.3 g/kg and 3 g/kg, p.o.), danshen (3 g/kg, p.o.) or gegen (3 g/kg, p.o.) for 7 days had no effect on blood pressure. However, the 7 days treatment with DG (3 g/kg) restored superoxide dismutase (SOD) and catalase (CAT) activities, suppressed the production of maleic dialdehyde (MDA), and inhibited the production of nitric oxide (NO). In addition, gegen (3 g/kg) restored SOD enzyme activity, whereas, danshen (3 g/kg) inhibited NO production. In addition, treatment with DG (3 g/kg) showed a significant reduction in infarct weight and improved the neurological deficit in a rat model of focal cerebral ischaemia induced by middle cerebral artery occlusion (MCAO). / In conclusion, the vasorelaxant actions of DG, danshen, gegen, salvianolic acid B, danshensu, daidzein and daidzin were found to involve the opening of K⁺ channels and inhibition of Ca²⁺ influx in the vascular smooth muscle cells. In contrast, puerarin produced vasodilatation via an endothelium-dependent mechanism involving NO production and an endothelium-independent pathway mediated by the opening of K⁺ channels. DG may have some cerebro-protective effects. Overall, the present studies showed that DG and its constituents could be beneficial to patients with obstructive cerebrovascular diseases. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Deng, Yan. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 164-178). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese. / ABSTRACT --- p.v / 摘要 --- p.iviii / ACKNOWLEDGEMENTS --- p.x / PUBLICATIONS BASED ON THIS THESIS --- p.xii / ABBREVIATIONS --- p.xiv / Chapter CHAPTER 1 --- Introduction --- p.1 / Chapter 1.1 --- Chinese Medicines in treatment of cerebrovascular diseases --- p.2 / Chapter 1.2 --- Danshen --- p.4 / Chapter 1.2.1 --- Chemical constituents --- p.4 / Chapter 1.2.1.1 --- Hydrophilic compounds of danshen --- p.4 / Chapter 1.2.1.2 --- Lipophilic compounds of danshen --- p.5 / Chapter 1.2.1.3 --- Other compounds --- p.5 / Chapter 1.2.2 --- Pharmacological activities --- p.5 / Chapter 1.2.2.1 --- Vascular protection --- p.5 / Chapter 1.2.2.2 --- Anti-tumour --- p.7 / Chapter 1.2.2.3 --- Treatment of liver diseases --- p.8 / Chapter 1.2.2.4 --- Treatment of drug addiction --- p.9 / Chapter 1.2.2.5 --- Treatment of kidney diseases --- p.10 / Chapter 1.2.3 --- Pharmacokinetics --- p.10 / Chapter 1.3 --- Gegen --- p.12 / Chapter 1.3.1 --- Chemical constituents --- p.12 / Chapter 1.3.2 --- Pharmacology --- p.13 / Chapter 1.3.2.1 --- Vascular effects --- p.13 / Chapter 1.3.2.2 --- Anti-diabetes --- p.14 / Chapter 1.3.2.3 --- Anti-hypercholesterolaemia --- p.15 / Chapter 1.3.2.4 --- Anti-inflammation --- p.16 / Chapter 1.3.2.5 --- Anti-platelet aggregation --- p.17 / Chapter 1.3.3 --- Pharmacokinetics --- p.17 / Chapter 1.4 --- Danshen and gegen formulation --- p.19 / Chapter 1.5 --- Mechanisms of vasodilatation --- p.22 / Chapter 1.5.1 --- Endothelium derived relaxant factors (EDRFs) --- p.22 / Chapter 1.5.1.1 --- Nitric oxide (NO) --- p.22 / Chapter 1.5.1.2 --- Prostacyclin (PGI₂) --- p.23 / Chapter 1.5.1.3 --- Endothelium-derived hyperpolarizating factors (EDHFs)- --- p.23 / Chapter 1.5.2 --- Signal transduction pathways --- p.24 / Chapter 1.5.2.1 --- Guanylyl cyclase-cGMP pathway --- p.24 / Chapter 1.5.2.2 --- Adenylyl cyclase-cAMP pathway --- p.24 / Chapter 1.5.3 --- Ion channels --- p.25 / Chapter 1.5.3.1 --- Potassium channels (K⁺ channels) --- p.25 / Chapter 1.5.3.2 --- Calcium channel (Ca²⁺ channels) --- p.25 / Chapter 1.6 --- Aims of study --- p.27 / Chapter CHAPTER 2 --- Materials and method --- p.28 / Chapter 2.1 --- Herbal preparation --- p.28 / Chapter 2.1.1 --- DG, danshen and gegen preparation --- p.28 / Chapter 2.1.2 --- Identification and quantification of chemical markers in DG water extract --- p.29 / Chapter 2.2 --- Experiments on rat basilar artery --- p.30 / Chapter 2.2.1 --- Animals --- p.30 / Chapter 2.2.2 --- Chemicals --- p.30 / Chapter 2.2.3 --- Isolation and mounting of blood vessels --- p.33 / Chapter 2.2.4 --- Protocols --- p.34 / Chapter 2.2.4.1 --- Effects on U46619-precontracted tone --- p.34 / Chapter 2.2.4.2 --- Endothelium-dependent mechanism --- p.34 / Chapter 2.2.4.3 --- Endothelium-independent mechanism --- p.35 / Chapter 2.2.4.4 --- Calcium channels --- p.36 / Chapter 2.2.4.5 --- Positive control --- p.36 / Chapter 2.2.5 --- Statistical analysis --- p.37 / Chapter 2.3 --- Experiments on rat cerebral basilar artery smooth muscle cells K[subscript ATP] channals --- p.38 / Chapter 2.3.1 --- Animals --- p.38 / Chapter 2.3.2 --- Chemicals --- p.38 / Chapter 2.3.3 --- Isolation of rat cerebral vascular smooth muscle cells --- p.40 / Chapter 2.3.4 --- Whole cell patch-clamp electrophysiology --- p.40 / Chapter 2.3.5 --- Statistical analysis --- p.44 / Chapter 2.4 --- Experiments on rat cerebral basilar artery smooth muscle cells calcium channels --- p.45 / Chapter 2.4.1 --- Animals --- p.45 / Chapter 2.4.2 --- Chemicals --- p.45 / Chapter 2.4.3 --- Isolation of rat cerebral vascular smooth muscle cells --- p.47 / Chapter 2.4.4 --- Dye loading and determination of [Ca²⁺]i --- p.47 / Chapter 2.4.5 --- Statistical analysis --- p.48 / Chapter 2.5 --- In vivo study of global ischaemia --- p.49 / Chapter 2.5.1 --- Animals --- p.49 / Chapter 2.5.2 --- Drugs and chemicals --- p.49 / Chapter 2.5.3 --- Experimental protocols for global ischaemia --- p.49 / Chapter 2.5.4 --- Induction of global ischaemia --- p.50 / Chapter 2.5.5 --- Blood pressure measurement --- p.52 / Chapter 2.5.6 --- Measurement of cerebral blood flow --- p.52 / Chapter 2.5.7 --- Biochemical assessment --- p.53 / Chapter 2.5.7.1. --- Dissection and homogenization --- p.53 / Chapter 2.5.7.2. --- Measurement of malondialdehyde (MDA) --- p.53 / Chapter 2.5.7.3. --- Estimation of nitrite --- p.53 / Chapter 2.5.7.4 --- Superoxide dismutase activity (SOD) --- p.54 / Chapter 2.5.7.5 --- Reduced glutathione (GSH) --- p.54 / Chapter 2.5.7.6 --- Catalase (CAT) --- p.55 / Chapter 2.5.7.7 --- NOS activity --- p.55 / Chapter 2.5.7.8 --- Protein --- p.56 / Chapter 2.5.8 --- Statistical analysis --- p.56 / Chapter 2.6 --- In vivo study of focal ischaemia --- p.57 / Chapter 2.6.1 --- Animals --- p.57 / Chapter 2.6.2 --- Drugs and chemicals --- p.57 / Chapter 2.6.3 --- Experimental protocols for global ischaemia --- p.57 / Chapter 2.6.4 --- Focal cerebral ischaemia-reperfusion model --- p.57 / Chapter 2.6.5 --- Assessment of neurobehavioural changes --- p.59 / Chapter 2.6.6 --- Assessment of cerebral infarction --- p.60 / Chapter 2.6.7 --- Statistical analysis --- p.60 / Chapter CHAPTER 3 --- Results --- p.61 / Chapter 3.1 --- Identification and quantification of chemical markers in DG water extract --- p.61 / Chapter 3.2 --- Effects of DG and its constituents on rat cerebral basilar artery --- p.64 / Chapter 3.2.1 --- Investigations on endothelium-dependent mechanisms --- p.64 / Chapter 3.2.2 --- Investigations on endothelium-independent mechanisms --- p.68 / Chapter 3.2.3 --- Positive control --- p.86 / Chapter 3.2.3 --- Investigations on calcium channels --- p.88 / Chapter 3.3 --- Effects of DG and its constituents on rat cerebral basilar artery smooth muscle cells --- p.91 / Chapter 3.3.1 --- Effects of water crude-extracts of DG, danshen, and gegen on K[subscript ATP] channels --- p.91 / Chapter 3.3.2 --- Effects of active constituents of danshen hydrophilic fraction on K[subscript ATP] channels --- p.100 / Chapter 3.3.3 --- Effects of the major isoflavonoids of gegen on K[subscript ATP] channels --- p.105 / Chapter 3.4 --- Effects of DG and its constituents on calcium channels of basilar artery smooth muscle cells --- p.112 / Chapter 3.5 --- Effects of DG, danshen and gegen on rat global ischaemia --- p.117 / Chapter 3.5.1 --- Effects of DG, danshen and gegen on rats’ blood pressure and cerebral blood flow --- p.117 / Chapter 3.5.2 --- Effects of DG, danshen and gegen on lipid peroxidation --- p.120 / Chapter 3.5.3 --- Effects of DG, danshen and gegen on SOD activity --- p.120 / Chapter 3.5.4 --- Effects of DG, danshen and gegen on CAT activity --- p.120 / Chapter 3.5.5 --- Effects of DG, danshen and gegen on reduced GSH level --- p.121 / Chapter 3.5.6 --- Effects of DG, danshen and gegen on NOS system --- p.126 / Chapter 3.6 --- Effect of DG on rat focal ischaemia --- p.129 / Chapter 3.6.1 --- Effect of DG on cerebral infarction --- p.129 / Chapter 3.6.2 --- Effect of DG on neurological deficits --- p.129 / Chapter CHAPTER 4 --- Discussion --- p.132 / Chapter 4.1 --- Studies of DG and its constituents on rat cerebral basilar artery --- p.133 / Chapter 4.1.1 --- Constituents of DG on U46619-precontracted tone --- p.133 / Chapter 4.1.2 --- Investigations on endothelium-dependent mechanisms --- p.133 / Chapter 4.1.3 --- Investigations on endothelium-independent mechanisms --- p.136 / Chapter 4.1.4 --- Investigations on calcium channels --- p.139 / Chapter 4.2 --- Effects of DG and its constituents on rat cerebral basilar artery smooth muscle cell K[subscript ATP] channels --- p.143 / Chapter 4.3 --- Effects of DG and its constituents on calcium influx in rat basilar artery smooth muscle cells --- p.147 / Chapter 4.4 --- Effects of DG, danshen and gegen on rat transient global ischaemia --- p.150 / Chapter 4.4.1 --- Effects of DG, danshen and gegen on rats’ blood pressure and cerebral blood flow --- p.150 / Chapter 4.4.2 --- Effects of DG, danshen and gegen on lipid peroxidation, SOD and CAT activity, and GSH level --- p.152 / Chapter 4.4.3 --- Effects of DG, danshen and gegen on NOS system --- p.155 / Chapter 4.5 --- Effects of DG on rat focal ischaemia --- p.157 / Chapter 4.6 --- Further studies --- p.160 / Chapter 4.7 --- Conclusion --- p.162 / REFERENCES --- p.164

In a mouse model of pulmonary thromboembolism induced by a collagen-adrenaline mixture, the SFE extract and ligustilide reduced the paralysis-death ratio, and the anti-thrombotic response of senkyunolide A was more pronounced. The effect of BDPH was not significant. Neither the SFE extract nor the three phthalides prolonged bleeding time in tail-transected mice. / In a rat myocardial ischemia-reperfusion model involving coronary artery ligation, 7-day pre-treatment with the SFE extract and ligustilide reduced ventricular arrhythmias in isolated hearts. BDPH and senkyunolide A were without significant effects. / In rat platelet-rich plasma, platelet aggregation induced by collagen and U46619 but not by adenosine diphosphate was inhibited by the SFE extract. Ligustilide inhibited the responses of all three agonists, while BDPH and senkyunolide A inhibited the collagen response only. / Raw Rhizoma Chuanxiong herb and its crude extract as obtained by supercritical fluid extraction (SFE) comprised mainly phthalides. The SFE extract and three representative phthalides, butylidenephthalide (BDPH), ligustilide and senkyunolide A, were studied on vasorelaxation, myocardial ischemia, platelet aggregation and thrombosis. The mechanisms underlying BDPH-mediated vasorelaxation were also explored. / Rhizoma Chuanxiong, the dried rhizome of Ligusticum chuanxiong Hort., is a common traditional Chinese medicine used for the treatment of cardiovascular diseases. Surprisingly, the scientific basis of its action is poorly understood. The current study aims to establish the pharmacological basis of the cardiovascular effects of Rhizoma Chuanxiong and its active constituents by examining their effects in several cardiovascular domains. / The current study demonstrated various cardiovascular actions of Rhizoma Chuanxiong, and thereby established the pharmacological basis of the effects of the herb. Phthalides, in particular BDPH, ligustilide and senkyunolide A, were important contributors to such actions. Future investigation of the SFE extract and/or individual phthalides related to the progression from in vitro and in vivo effectiveness to clinical efficacy is much anticipated. / The SFE extract, BDPH, ligustilide and senkyunolide A produced vasorelaxation on isolated preparations of rat aorta, rat saphenous vein and pig coronary artery. BDPH-mediated relaxation appeared to involve both extracellular Ca 2+-dependent (L-type voltage-operated, receptor-operated and store-operated Ca2+ channels) and independent (NO modulation, Ca2+ release from internal stores and Ca2+ desensitization) mechanisms. BDPH was also observed to augment relaxation induced by sodium nitroprusside and forskolin through mechanisms that remain undefined. / Chan Sun Kin Sunny. / "July 2005." / Advisers: G. Lin; R. L. Jones. / Source: Dissertation Abstracts International, Volume: 68-03, Section: B, page: 1575. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (p. 190-209). / 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.

Ng Chi Ho. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (leaves 147-160). / Abstracts in English and Chinese. / ACKNOWLEDGMENTS --- p.I / ABSTRACT --- p.II / LIST OF ABBREVIATIONS --- p.VII / TABLE OF CONTENTS --- p.IX / Chapter CHAPTER 1 --- GENERAL INTRODUCTION / Chapter 1.1 --- Introduction of Low-density lipoprotein --- p.1 / Chapter 1.1.1 --- What are lipids? --- p.1 / Chapter 1.1.2 --- Function and structure of cholesterol --- p.1 / Chapter 1.1.3 --- Function and classification of lipoprotein --- p.1 / Chapter 1.2 --- Functions of low-density lipoprotein --- p.2 / Chapter 1.3 --- Basic structure of low-density lipoprotein --- p.4 / Chapter 1.4 --- Principle on isolation and purification of low-density lipoprotein --- p.4 / Chapter 1.5 --- Cholesterol transport system --- p.7 / Chapter 1.5.1 --- Exogenous pathway of cholesterol metabolism --- p.7 / Chapter 1.5.2 --- Endogenous pathway of cholesterol metabolism --- p.7 / Chapter 1.5.3 --- Reverse transport of Cholesterol --- p.8 / Chapter 1.6 --- Oxidation of LDL --- p.10 / Chapter 1.6.1 --- Agents that causes oxidation --- p.10 / Chapter 1.6.1.1 --- Lipoxygenases --- p.10 / Chapter 1.6.1.2 --- Myeloperoxidase --- p.10 / Chapter 1.6.1.3 --- Reactive nitrogen species --- p.11 / Chapter 1.6.1.4 --- Reactive oxygen species --- p.11 / Chapter 1.6.2 --- Factors that affect the susceptibility of LDL oxidation --- p.13 / Chapter 1.7 --- Hyperlipidaemia 一 chance to increase LDL oxidation --- p.13 / Chapter 1.7.1 --- Definition of hyperlipidemia and hypercholesterolemia --- p.13 / Chapter 1.7.2 --- Risk factors of hyperlipidaemia --- p.13 / Chapter 1.7.2.1 --- High fat low fibre diets: --- p.13 / Chapter 1.7.2.2 --- Obesity --- p.14 / Chapter 1.7.2.3 --- Type II diabetes --- p.14 / Chapter 1.7.2.4 --- Genetic factors (Familial hyperlipidemias) --- p.14 / Chapter 1.8 --- Diseases related to oxidized LDL --- p.15 / Chapter 1.8.1 --- Cardiovascular diseases --- p.15 / Chapter 1.8.1.1 --- Atherosclerosis and ischemic heart attack --- p.15 / Chapter 1.8.1.2 --- Factors that affect incidence of atherosclerosis --- p.16 / Chapter 1.8.1.2.1 --- Triglyceride-rich lipoprotein --- p.16 / Chapter 1.8.1.2.2 --- Small and dense LDL --- p.16 / Chapter 1.8.1.3 --- Stroke --- p.17 / Chapter 1.8.2 --- Common ways to reduce plasma cholesterol level --- p.17 / Chapter 1.8.2.1 --- Diet control --- p.17 / Chapter 1.8.2.2 --- Physical activity --- p.17 / Chapter 1.8.2.3 --- Drug therapy --- p.18 / Chapter CHAPTER 2 --- IMPAIRMENT OF OXIDIZED LDL ON ENDOTHELIUM-DEPENDENT RELAXATION / Chapter 2.1 --- Introduction --- p.19 / Chapter 2.1.1 --- Properties and function of phenylephrine hydrochloride --- p.22 / Chapter 2.1.2 --- Properties and function of acetylcholine --- p.22 / Chapter 2.2 --- Objectives --- p.23 / Chapter 2.3 --- Materials and methods --- p.24 / Chapter 2.3.1 --- Preparation of drugs --- p.24 / Chapter 2.3.2 --- Preparation of human native LDL --- p.25 / Chapter 2.3.3 --- Preparation of oxidized LDL --- p.27 / Chapter 2.3.4 --- Preparation of aorta --- p.27 / Chapter 2.3.5 --- Measurement of Isometric Force in vitro --- p.30 / Chapter 2.3.5.1 --- Protocol 1- Dose effect of oxidized LDL on acetylcholine-induced vasorelaxation --- p.30 / Chapter 2.3.5.2 --- Protocol 2 - Time effect of oxidized LDL on acetylcholine-induced vasorelaxation --- p.30 / Chapter 2.3.5.3 --- Protocol 3 - Effect of co-incubation of LDL and copper(ll) sulphate on acetylcholine-induced vasorelaxation --- p.31 / Chapter 2.3.5.4 --- Protocol 4 - Effect of oxidized LDL on selected vasodilators --- p.32 / Chapter 2.3.5.5 --- Protocol 5 - Effect of pretreatment of L-arginine on oxidized LDL impaired -endothelium-induced relaxation --- p.32 / Chapter 2.3.5.6 --- Protocol 6 - Effect of a -tocopherol on oxidized LDL-damaged acetylcholine- induced vasorelaxation --- p.33 / Chapter 2.3.5.7 --- Protocol 7 - Effect of a -tocopherol on LDL and copper(ll) sulphate- induced endothelial dysfunction --- p.33 / Chapter 2.3.6 --- Western blot analysis of endothelial nitric oxide synthase (eNOS) protein --- p.34 / Chapter 2.3.7 --- Statistics --- p.35 / Chapter 2.4 --- Results --- p.36 / Chapter 2.4.1 --- Dose effect of oxidized LDL on acetylcholine-induced vasorelaxation --- p.36 / Chapter 2.4.2 --- Time effect of oxidized LDL on acetylcholine-induced vasorelaxation --- p.36 / Chapter 2.4.3 --- Effect of co-incubation of LDL and copper(II) sulphate on acetylcholine- induced vasorelaxation --- p.39 / Chapter 2.4.4 --- Effect of oxidized LDL on selected vasodilators --- p.41 / Chapter 2.4.5 --- Effect of pretreatment of L-arginine on oxidized LDL impaired- acetylcholine-induced relaxation --- p.41 / Chapter 2.4.6 --- Effect of a-tocopherol on oxidized LDL-damaged acetylcholine- induced vasorelaxation --- p.48 / Chapter 2.4.7 --- Effect of a-tocopherol on LDL and copper(II) sulphate-induced endothelial dysfunction --- p.50 / Chapter 2.4.8 --- eNOS Protein expression --- p.50 / Chapter 2.5 --- Discussion --- p.53 / Chapter CHAPTER 3 --- EFFECTS OF LDL INJECTION ON THE ENDOTHELIAL FUNCTION OF RATS / Chapter 3.1 --- Introduction --- p.58 / Chapter 3.2 --- Objective --- p.60 / Chapter 3.3 --- Methods and Materials --- p.61 / Chapter 3.3.1 --- Preparation of Drugs --- p.61 / Chapter 3.3.2 --- Preparation of LDL --- p.61 / Chapter 3.3.3 --- Animal Treatment --- p.61 / Chapter 3.3.4 --- Serum lipid and lipoprotein determinations --- p.62 / Chapter 3.3.5 --- Measurement of serum MDA level by TBARS assay --- p.62 / Chapter 3.3.6 --- Preparation of aorta --- p.62 / Chapter 3.3.7 --- Organ bath experiment --- p.63 / Chapter 3.3.8 --- Statistics --- p.64 / Chapter 3.4 --- Result --- p.65 / Chapter 3.4.1 --- Growth and food intake --- p.65 / Chapter 3.4.2 --- "Effect of LDL injection on serum TC, TG and HDL-C" --- p.65 / Chapter 3.4.3 --- Effect of LDL injection on non-HDL-C and ratio of non-HDL-C to HDL-C --- p.65 / Chapter 3.4.4 --- Serum MDA level --- p.68 / Chapter 3.4.5 --- Phenylephrine-induced contraction --- p.70 / Chapter 3.4.6 --- Endothelium-dependent and -independent relaxation --- p.75 / Chapter 3.5 --- Discussion --- p.79 / Chapter CHAPTER 4 --- EFFECTS OF INDIVIDUAL COMPONENT OF OXIDIZED LDL ON ENDOTHELIUM-DEPENDENT RELAXATION / Chapter 4.1 --- Introduction --- p.83 / Chapter 4.2 --- Objectives --- p.85 / Chapter 4.3 --- Materials and methods --- p.86 / Chapter 4.3.1 --- Preparation of drugs --- p.86 / Chapter 4.3.2 --- Preparation of human native LDL and oxidized LDL --- p.86 / Chapter 4.3.3 --- GC analysis of fatty acid composition in LDL --- p.86 / Chapter 4.3.4 --- TBARS assay analysis of MDA content in LDL --- p.87 / Chapter 4.3.5 --- GC analysis of cholesterol oxidation products in LDL --- p.89 / Chapter 4.3.6 --- Thin-layer chromatography analysis of LPC in LDL --- p.91 / Chapter 4.3.7 --- Preparation of aorta --- p.92 / Chapter 4.3.8 --- Measurement of Isometric Force in vitro --- p.92 / Chapter 4.3.8.1 --- Protocol 1- effect of LPC on acetylcholine-induced vasorelaxation --- p.92 / Chapter 4.3.8.2 --- Protocol 2- effect of cholesterol oxidation products on acetylcholine-induced vasorelaxation --- p.92 / Chapter 4.3.8.3 --- Protocol 3- effect of oxidized fatty acids on acetylcholine-induced vasorelaxation --- p.93 / Chapter 4.3.9 --- Statistics --- p.93 / Chapter 4.4 --- Results --- p.94 / Chapter 4.4.1 --- Compositional differences between native LDL and oxidized LDL.… --- p.94 / Chapter 4.4.2 --- Effect of LPC on endothelium-dependent relaxation --- p.98 / Chapter 4.4.3 --- Effect of COPs on endothelium-dependent relaxation --- p.98 / Chapter 4.4.4 --- Effect of oxidized fatty acids on endothelium-dependent relaxation --- p.101 / Chapter 4.5 --- Discussion --- p.103 / Chapter CHAPTER 5 --- EFFECTS OF DIETARY OXIDIZED CHOLESTEROL ON BLOOD CHOLESTEROL LEVEL IN HAMSTERS / Chapter 5.1 --- Introduction --- p.107 / Chapter 5.2 --- Objectives --- p.111 / Chapter 5.3 --- Materials and Methods --- p.112 / Chapter 5.3.1 --- Preparation of Oxidized Cholesterol --- p.112 / Chapter 5.3.2 --- Diet preparation --- p.112 / Chapter 5.3.3 --- Animals --- p.113 / Chapter 5.3.4 --- Serum lipid and lipoprotein determinations --- p.116 / Chapter 5.3.5 --- GC analysis of cholesterol and cholesterol oxidation products on organs --- p.116 / Chapter 5.3.6 --- Extraction of neutral and acidic sterols from fecal samples --- p.117 / Chapter 5.3.6.1 --- Determination of neutral sterols --- p.117 / Chapter 5.3.6.2 --- Determination of acidic sterols --- p.117 / Chapter 5.3.6.3 --- GLC analysis of neutral and acidic sterols --- p.118 / Chapter 5.3.7 --- Organ bath experiment --- p.121 / Chapter 5.3.7.1 --- Preparation of aorta --- p.121 / Chapter 5.3.7.2 --- Aortic relaxation --- p.121 / Chapter 5.3.8 --- Analysis of the total area of atherosclerotic plaque on aorta --- p.122 / Chapter 5.3.9 --- Statistics --- p.122 / Chapter 5.4 --- Results --- p.123 / Chapter 5.4.1 --- GC of oxidized cholesterol --- p.123 / Chapter 5.4.2 --- Growth and food intake --- p.123 / Chapter 5.4.3 --- "Effect of non-oxidized and oxidized cholesterol on serum TC, TG and HDL-C" --- p.123 / Chapter 5.4.4 --- Effect of non-oxidized and oxidized cholesterol on non-HDL-C and ratio of non-HDL-C to HDL-C --- p.124 / Chapter 5.4.5 --- Effect ofnon-oxidized and oxidized cholesterol on concentration of hepatic cholesterol --- p.128 / Chapter 5.4.6 --- Effect of non-oxidized and oxidized cholesterol on concentration of cholesterol oxidation products accumulated in liver --- p.128 / Chapter 5.4.7 --- Effect of non-oxidized and oxidized cholesterol on concentration of brain and aortic cholesterol --- p.128 / Chapter 5.4.8 --- Effect of non-oxidized and oxidized cholesterol on fecal neutral and acidic sterols --- p.129 / Chapter 5.4.9 --- Effect of non-oxidized and oxidized cholesterol on aortic relaxation --- p.135 / Chapter 5.4.10 --- Effect of non-oxidzied and oxidized cholesterol on area of atherosclerotic plaque --- p.137 / Chapter 5.5 --- Discussion --- p.139 / Chapter CHAPTER 6 --- CONCLUSION --- p.143 / REFERENCES --- p.146