Chan, Yuet Wa. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2009. / Includes bibliographical references (leaves 217-232). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese.

O conhecimento de que o exercício é benéfico na doença aterosclerótica é baseado principalmente em estudos epidemiológicos. O objetivo deste trabalho foi investigar se o treinamento físico preventivo ou terapêutico altera a evolução da placa aterosclerótica. Camundongos LDLr-/- com 16 semanas de vida foram separados em dois programas: preventivo e terapêutico. Animais do programa preventivo receberam dieta normal ou aterogênica por 14 semanas. O treinamento físico foi iniciado concomitantemente ao início da dieta. Animais do programa terapêutico receberam dieta normal ou aterogênica por 28 semanas. O treinamento físico foi iniciado após 14 semanas do início da dieta, com placas bem estabelecidas. O treinamento físico aeróbico moderado foi realizado em esteira rolante, por 60 min, 5 dias/sem, durante 14 semanas. Massa corporal, pressão arterial caudal e freqüência cardíaca foram registradas. Lipoproteínas plasmáticas foram separadas por FPLC e colesterol total foi dosado por métodos enzimáticos. Foram quantificados tamanho, conteúdo de gordura e de colágeno da placa por coloração de oil-red O e picro-sirius. Citocinas TNF-, IL-6 foram medidas por Elisa. MMP-9 plasmática foi medida por zimografia. Marcadores inflamatórios teciduais, MMP-9, CD40/CD40L e nitrotirosina, foram medidos na placa por imunohistoquímica. O treinamento físico não modificou o tamanho da placa, mas tornou a placa mais estável por aumentar o conteúdo de colágeno. O treinamento físico diminuiu o conteúdo de gordura da placa, os fatores de risco e o CD40 somente no programa preventivo. Nenhuma alteração foi notada nos marcadores inflamatórios circulantes e na expressão de MMP-9 e formação de nitrotirosina na placa aterosclerótica. / The knowledge that exercise exerts beneficial effects on atherosclerotic disease is mainly based on epidemiological studies. Our aim was to investigate the effect of preventive and therapeutic exercise programs on atherosclerotic plaque formation and development. Sixteen-week-old LDLr-/- mice were randomly divided into preventive and therapeutic programs. Preventive programs mice received normal or atherogenic diet for 14 weeks. Exercise training started at the same time of dieting. Therapeutic programs mice received normal or atherogenic diet for 28 weeks. Exercise training started after 14 weeks of dieting when atherosclerosis plaques were already established. Moderate intensity aerobic exercise training was performed on a motor treadmill for 60 min, 5 days/wk, during 14 weeks. Body mass, caudal blood pressure and heart rate were registered. Plasma lipoproteins were separated by FPLC and total cholesterol was determined by enzymatic methods. Cross sections of aortic root were stained with oil-red O for plaque size and fat content. Aorta longitudinal sections were stained with picro-sirius for collagen content. TNF- and IL-6 cytokines were measured by Elisa. Plasmatic MMP-9 was determined by zimography. Inflammatory tissue markers, MMP-9, CD40/CD40L and nitrotirosine, were measured by immunohistochemistry. We concluded that exercise training did not modify plaque size, but turned it into a more stable one by increasing its collagen content. Exercise training reduced plaque fat content, risk factors and plaque CD40 expression only in the preventive program. No difference in systemic inflammatory markers, and in plaque MMP-9 expression and nitrotirosine formation was noted.

O conhecimento de que o exercício é benéfico na doença aterosclerótica é baseado principalmente em estudos epidemiológicos. O objetivo deste trabalho foi investigar se o treinamento físico preventivo ou terapêutico altera a evolução da placa aterosclerótica. Camundongos LDLr-/- com 16 semanas de vida foram separados em dois programas: preventivo e terapêutico. Animais do programa preventivo receberam dieta normal ou aterogênica por 14 semanas. O treinamento físico foi iniciado concomitantemente ao início da dieta. Animais do programa terapêutico receberam dieta normal ou aterogênica por 28 semanas. O treinamento físico foi iniciado após 14 semanas do início da dieta, com placas bem estabelecidas. O treinamento físico aeróbico moderado foi realizado em esteira rolante, por 60 min, 5 dias/sem, durante 14 semanas. Massa corporal, pressão arterial caudal e freqüência cardíaca foram registradas. Lipoproteínas plasmáticas foram separadas por FPLC e colesterol total foi dosado por métodos enzimáticos. Foram quantificados tamanho, conteúdo de gordura e de colágeno da placa por coloração de oil-red O e picro-sirius. Citocinas TNF-, IL-6 foram medidas por Elisa. MMP-9 plasmática foi medida por zimografia. Marcadores inflamatórios teciduais, MMP-9, CD40/CD40L e nitrotirosina, foram medidos na placa por imunohistoquímica. O treinamento físico não modificou o tamanho da placa, mas tornou a placa mais estável por aumentar o conteúdo de colágeno. O treinamento físico diminuiu o conteúdo de gordura da placa, os fatores de risco e o CD40 somente no programa preventivo. Nenhuma alteração foi notada nos marcadores inflamatórios circulantes e na expressão de MMP-9 e formação de nitrotirosina na placa aterosclerótica. / The knowledge that exercise exerts beneficial effects on atherosclerotic disease is mainly based on epidemiological studies. Our aim was to investigate the effect of preventive and therapeutic exercise programs on atherosclerotic plaque formation and development. Sixteen-week-old LDLr-/- mice were randomly divided into preventive and therapeutic programs. Preventive programs mice received normal or atherogenic diet for 14 weeks. Exercise training started at the same time of dieting. Therapeutic programs mice received normal or atherogenic diet for 28 weeks. Exercise training started after 14 weeks of dieting when atherosclerosis plaques were already established. Moderate intensity aerobic exercise training was performed on a motor treadmill for 60 min, 5 days/wk, during 14 weeks. Body mass, caudal blood pressure and heart rate were registered. Plasma lipoproteins were separated by FPLC and total cholesterol was determined by enzymatic methods. Cross sections of aortic root were stained with oil-red O for plaque size and fat content. Aorta longitudinal sections were stained with picro-sirius for collagen content. TNF- and IL-6 cytokines were measured by Elisa. Plasmatic MMP-9 was determined by zimography. Inflammatory tissue markers, MMP-9, CD40/CD40L and nitrotirosine, were measured by immunohistochemistry. We concluded that exercise training did not modify plaque size, but turned it into a more stable one by increasing its collagen content. Exercise training reduced plaque fat content, risk factors and plaque CD40 expression only in the preventive program. No difference in systemic inflammatory markers, and in plaque MMP-9 expression and nitrotirosine formation was noted.

Cheung, Wing Shing David. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2013. / Includes bibliographical references (leaves 201-217). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Ng, Chun Fai. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 134-150). / Abstracts in English and Chinese. / Abstract --- p.i / Acknowledgements --- p.vii / Table of Contents --- p.ix / Abbreviations --- p.xii / List of Figures --- p.xv / List of Tables --- p.xviii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- "Introduction to Cardiovascular Disease, Hypertension and Atherosclerosis" --- p.1 / Chapter 1.1.1 --- Cardiovascular Disease --- p.1 / Chapter 1.1.2 --- Hypertension --- p.2 / Chapter 1.1.2.1 --- Background --- p.2 / Chapter 1.1.2.2 --- Causes of Hypertension --- p.3 / Chapter 1.1.2.3 --- Current Western Management and Medication --- p.6 / Chapter 1.1.3 --- Atherosclerosis --- p.9 / Chapter 1.1.3.1 --- Background --- p.9 / Chapter 1.1.3.2 --- Pathogenesis of Atherosclerosis --- p.10 / Chapter 1.1.3.3 --- Current Western Treatment and Medication --- p.12 / Chapter 1.2 --- Selection and Introduction of Current Chinese Medicine Formula --- p.16 / Chapter 1.2.1 --- Cardiac Syndrome in Traditional Chinese Medicine --- p.16 / Chapter 1.2.2 --- Traditional Chinese Medicine as an Complementary or Alternative Medicine --- p.17 / Chapter 1.2.3 --- Selection of TCM Formula from Pharmacopoeia --- p.18 / Chapter 1.2.3.1 --- Compound Formula --- p.18 / Chapter 1.2.4 --- Introduction to Constitutional Herbal Medicine --- p.19 / Chapter 1.2.4.1 --- Danshen (Radix Salviae miltiorrhizae) --- p.19 / Chapter 1.2.4.2 --- Gegen (Radix Puerariae lobatae) --- p.20 / Chapter 1.2.4.3 --- Yanhusuo (Rhizoma Corydalis) --- p.21 / Chapter 1.2.4.4 --- Composition of the Final Formula Used in the Present Study --- p.21 / Chapter 1.2.5 --- Previous work on Danshen-Gegen Formula and its limitations --- p.22 / Chapter 1.3 --- Objectives of the Present Study --- p.25 / Chapter 1.3.1 --- Research Plan --- p.26 / Chapter Chapter 2 --- Experimental Design and General Methodology --- p.27 / Chapter 2.1 --- Source and Authentication of Raw Herbs --- p.27 / Chapter 2.2 --- Materials --- p.29 / Chapter 2.3 --- Ethical Approval --- p.31 / Chapter 2.4. --- General Methods --- p.32 / Chapter 2.4.1 --- Blood Pressure Measurement --- p.32 / Chapter 2.4.2 --- Blood Profile Measurement --- p.33 / Chapter 2.4.3 --- Vascular Reactivity Studies --- p.36 / Chapter 2.5 --- Statistical Analysis --- p.38 / Chapter Chapter 3 --- Anti-hypertensive Studies of Danshen-Gegen Formula on Rat --- p.39 / Chapter 3.1 --- Introduction --- p.39 / Chapter 3.1.1 --- In vivo Anti-Hypertensive Studies --- p.39 / Chapter 3.1.1.1 --- Spontaneously Hypertensive Rat (SHR) --- p.40 / Chapter 3.1.1.2 --- Tail-cuff Blood Pressure Measurement --- p.41 / Chapter 3.1.2 --- Detailed Underlying Mechanistic Studies --- p.42 / Chapter 3.1.2.1 --- Nitric Oxide-mediated Vasodilation --- p.42 / Chapter 3.1.2.2 --- Prostacyclin-mediated Vasodilation --- p.43 / Chapter 3.1.2.3 --- Hyperpolarization-mediated Vasodilation --- p.43 / Chapter 3.1.2.4 --- Endothelium-dependent/-independent Vasodilation --- p.46 / Chapter 3.1.3 --- Long Term Underlying Mechanistic Studies --- p.48 / Chapter 3.2 --- Methods --- p.49 / Chapter 3.2.1 --- In vivo Anti-Hypertensive Studies --- p.49 / Chapter 3.2.2 --- Detailed Underlying Mechanistic Studies --- p.51 / Chapter 3.2.3 --- Long Term Underlying Mechanistic Studies --- p.53 / Chapter 3.2.4 --- Statistical analysis --- p.56 / Chapter 3.3 --- Results --- p.58 / Chapter 3.3.1 --- In vivo Anti-Hypertensive Studies --- p.58 / Chapter 3.3.1.1 --- Preventive Effect in Hypertension --- p.58 / Chapter 3.3.1.2 --- Therapeutic Effect in Hypertension --- p.62 / Chapter 3.3.2 --- Detailed Underlying Mechanistic Studies --- p.66 / Chapter 3.3.2.1 --- DG extract-induced Vasodilation --- p.66 / Chapter 3.3.2.2 --- Endothelium-independent Vasodilation --- p.67 / Chapter 3.3.2.3 --- Nitric Oxide-mediated Vasodilation --- p.68 / Chapter 3.3.2.4 --- Prostacyclin-mediated Vasodilation --- p.69 / Chapter 3.3.2.5 --- Hyperpolarization-mediated Vasodilation --- p.70 / Chapter 3.3.3 --- Long Term Underlying Mechanistic Studies --- p.74 / Chapter 3.4 --- Discussion --- p.79 / Chapter Chapter 4 --- Anti-atherosclerosis Studies of Danshen-Gegen Formula in Rabbits --- p.89 / Chapter 4.1 --- Introduction --- p.89 / Chapter 4.1.1 --- Intima-Media Thickening --- p.89 / Chapter 4.1.2 --- Effect of High Cholesterol Diet in Rabbit --- p.90 / Chapter 4.1.3 --- Thiobarbituric Acid Reactive Substances --- p.91 / Chapter 4.2 --- Methods --- p.93 / Chapter 4.2.1 --- Pilot Study for Establishment of Experimental Protocol --- p.93 / Chapter 4.2.2 --- Effect of DG extract on Intima-media Thickening --- p.97 / Chapter 4.2.3 --- Statistical analysis --- p.99 / Chapter 4.3 --- Result --- p.100 / Chapter 4.3.1 --- Study of the Anti-atherosclerosis Effect of DG extract - First Run --- p.100 / Chapter 4.3.2 --- Study of the Anti-atherosclerosis Effect of DG extract - Second Run --- p.108 / Chapter 4.4 --- Discussion --- p.117 / Chapter Chapter 5 --- General Discussion and Conclusion --- p.122 / Chapter 5.1 --- Significance of the Study --- p.122 / Chapter 5.2 --- Limitations and Future work --- p.127 / Chapter 5.3 --- Clinical Implication of the Use of the DG Preparations for Patients with CVD --- p.132 / References --- p.134

University of Macau / Institute of Chinese Medical Sciences