For cardiotonic actions, DF caused a transient increase in contractility and a transient decrease in contraction rate in an isolated rat heart perfusion system. The positive inotropic effect and the negative chronotropic effect were generated by the dose-dependent inhibitions of Na+/K +-ATPase and Ca2+-ATPase respectively in rat heart homogenate. In both assays, Danshen exhibited more potent inhibitions than DF, while Fenge showed negligible inhibitory actions. / In vivo study on Spontaneously Hypertensive Rats (SHR) showed that DF could not restore the established high blood pressure to the normal level. Earlier DF treatment attenuated, but could not prevent, hypertension development. In aorta, DF improved endothelium-dependent vasodilation by potentiating acetylcholine-induced relaxation and basal nitric oxide (NO) production, and inhibiting endothelial Ca2+ATPases. Relaxation of vascular smooth muscle cells (VSMC) towards NO donors was also enhanced. For anti-oxidation, upon DF treatment, mRNA levels of superoxide dismutase (SOD), extracellular superoxide dismutase (ecSOD), catalase and glutathione peroxidase (GPx) were elevated in heart and aorta. However, studies on SOD and catalase demonstrated insignificant changes in the protein expression levels in both organs. For vasodilation, mRNA level of endothelial nitric oxide synthase (eNOS) in the aorta was upregulated, but no change on eNOS and phosphorylated eNOS (peNOS) proteins were detected. A parallel study showed that DF did not cause hypotension or improve antioxidant defense in normotensive Wistar Kyoto rats (WKY). These findings suggest the use of the Danshen and Fenge 7:3 (w/w) formulation on the comprehensive cardiovascular protection. / Previously established Danshen and Fenge 7:3 (w/w) formulation (DF) was shown to exhibit antioxidative activity by preventing oxidant-induced red blood cell hemolysis and H9c2 rat myoblast cell death in a dose-dependent manner, in which Danshen was demonstrated to be a more potent antioxidant than DF. Fenge showed no antioxidative property. The effect of in vivo ischemia-reperfusion was mimicked by the hypoxia-reoxygenation model of primary culture of neonatal rat heart cardiomyocytes. Danshen could protect cardiomyocytes against hypoxiareoxygenation damage. / Reactive oxygen species attack on cardiovascular system can lead to atherosclerosis and finally cardiac ischemia. Reperfusion, allowing the restoration of blood flow in treating atherosclerosis, in turn generates free radicals which irreversibly damage cardiomyocytes and endothelial cells. Endothelial cell damage eventually leads to hypertension. Radix Salviae Miltiorrhizae (Danshen) and Radix Puerariae Thomsonii (Fenge) have long been used together to treat various heart diseases in China. This project was focused on the antioxidative, cardiotonic and vasodilative effects of the aqueous extracts of Danshen and Fenge. / Lam Hung Ming. / "September 2006." / Adviser: Miu Yee Mary Waye. / Source: Dissertation Abstracts International, Volume: 68-03, Section: B, page: 1381. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (p. 218-230). / 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.
Identifer | oai:union.ndltd.org:cuhk.edu.hk/oai:cuhk-dr:cuhk_343909 |
Date | January 2006 |
Contributors | Lam, Hung Ming., Chinese University of Hong Kong Graduate School. Division of Biochemistry. |
Source Sets | The Chinese University of Hong Kong |
Language | English, Chinese |
Detected Language | English |
Type | Text, theses |
Format | electronic resource, microform, microfiche, 1 online resource (xxviii, 230 p. : ill.) |
Coverage | China, China |
Rights | Use of this resource is governed by the terms and conditions of the Creative Commons “Attribution-NonCommercial-NoDerivatives 4.0 International” License (http://creativecommons.org/licenses/by-nc-nd/4.0/) |
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