Thesis (M.S.)--Oregon State University, 2007. / Printout. Includes bibliographical references (leaves 162-183). Also available on the World Wide Web.

Thesis (Ph. D.)--Ohio State University, 2004. / Title from first page of PDF file. Document formatted into pages; contains xvii, 274 p.; also includes graphics (some col.). Includes abstract and vita. Advisor: J. Schwartzbaum, School of Public Health. Includes bibliographical references (p. 171-203).

Most studies on the antihypertensive effects of bioflavonoids have reported short-term effects (within 7 weeks) at high concentrations (40–100 mg kg–1 day–1). The present study by contrast has investigated long-term effects of low concentrations of bioflavonoids on arterial blood pressure and left ventricular performance in spontaneously hypertensive rats (SHR). Spontaneously hypertensive rats were divided into a treated (n = 16) and a control (n = 16) group. The treated group received daily a grape seed proanthocyanidin extract (GSPE) at a concentration of 4mg kg–1day–1over six months. Arterial blood pressure (ABP) was measured once monthly on six randomly selected rats from both groups using an indirect tail-cuff method. After three months, the remaining rats underwent catheterizations to measure left ventricular performance and aortic pressure. The possible role of nitric oxide (NO) in the effects of GSPE was investigated by blocking NO synthase with N-nitro-Larginine methyl ester (L-NAME). Animals in the treated group had significantly lower arterial end-diastolic pressures (AEDP) after three months of treatment compared with control animals, and this trend continued until six months. In the treated group, left ventricular systolic pressures (LVSP) were reduced by 16.6% (P = 0.005), their dP/dtmax (left ventricular pressures) were reduced by 19.7% (P = 0.050), and cardiac work was reduced by 22.0% (P = 0.045) at the end of three months. Treatment with L-NAMEsuggested a contribution of NO to the effects of GSPE on blood pressure. A low concentration of GSPE administered over six months lowered AEDP significantly, and the L-NAME response suggested that NO is involved. The decreased AEDP had a lowering effect on left ventricular dynamics of hypertensive rats.

Thesis (M.S.)--Oregon State University, 2011. / Printout. Includes bibliographical references (leaves 75-80). Also available on the World Wide Web.

Thesis (M.S.)--West Virginia University, 2005. / Title from document title page. Document formatted into pages; contains viii, 14, [22] p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.

Thesis (M.S.)--Rutgers University, 2008. / "Graduate Program in Animal Sciences." Includes bibliographical references (p. 48-51).

This thesis constitutes a report on a series of studies undertaken on possible mechanisms of action of the bioflavonoid, hesperidin methyl chalcone (HMC), in causing smooth muscle to relax. The term bioflavonoid refers to several compounds that can be extracted from the mesocarp of citrus fruits. They have been the subject of investigation and controversy since 1936. Much of this is covered in a eview by Vogin (1). As mentioned in the review, Szenti-Gyorgyi observed first that crude citrus extracts were more efficient in relieving experimental scurvy than pure extract containing only Vitamin C. The subject of scurvy has been covered in many reviews, and no purpose would be served in describing all these factors at this time. However, since Szent-Gyorgi’s observation, there has been considerable study of the possibility that bioflavonoids are a factor in capillary integrity. Despite all the activity, the necessity of bioflavonoids as a dietary adjuvant has not been established. At this date, almost thirty years after the initial studies, the literature is replete with contradictory statements on almost every phase of bioflavonoid activity. The possibility that HMC might have a direct action on smooth muscle indicated that both in vivo and in vitro studies should be utilized. The in vivo studies consisted of observations on blood pressure and nictitating membranes of cats. The in vitro studies were performed on sections of rabbit ileum.

The thesis describes the effects of various plant flavonoids (curcumin, epigallocatechin-3-gallate [EGCG], luteolin, apigenin, myricetin, quercetin, and cyanidin) on the physiological properties and viability of cultured human retinal pigment epithelial (RPE) cells. It is described that, with the exception of EGCG, all flavonoids tested decrease dose-dependently the RPE cell proliferation, migration, and secretion of VEGF. Luteolin, apigenin, myricetin, and quercetin decreased the viability of RPE cells at higher concentrations, by triggering cellular necrosis. Curcumin decreased the viability of RPE cells via induction of early necrosis and delayed apoptosis. The cytotoxic effect of curcumin involved activation of caspase-3 and calpain, intracellular calcium signaling, mitochondrial permeability, oxidative stress, and increased phosphorylation of p38 MAPK and decreased phosphorylation of Akt protein. Myricetin caused caspase-3 independent RPE cell necrosis mediated by free radical generation and activation of calpain and phospholipase A2. The myricetin- and quercetin-induced RPE cell necrosis was partially inhibited by necrostatin-1, a blocker of programmed necrosis. The author concludes that the intake of curcumin, luteolin, apigenin, myricetin, and quercetin as supplemental cancer therapy or in the treatment of retinal diseases should be accompanied by careful monitoring of the retinal function. Possible beneficial effects of EGCG and cyanidin in the treatment of retinal diseases should be examined in further investigations.

The effects of three oral dosages (0.4 mg, 0.8 mg, and 1.6 mg) of quercetin on Colon-25 tumors implanted in Balb-c mice were studied. The data in this study show that: (1) certain dosages of quercetin in alcohol solutions, reduces the weight, and size of implanted Colon-25 tumors in Balb-c mice, (2) these same dosages of quercetin all produce a profound neutrophilia combined with a significant lymphopenia at day 20 post-implantation, and (3) there was relatively little evidence of histological changes in the quercetin-treated tumor section which would indicate that the action(s) of quercetin is primarily at the subcellular level probably within the nuclei of the tumor cells.

Pan, Tak Yin. / Thesis submitted in: November 2007. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references. / Abstracts in English and Chinese. / Acknowledgements --- p.i / Abstract (English) --- p.ii / Abstract (Chinese) --- p.iv / Content --- p.v / Abbreviations --- p.x / List of Figures --- p.xi / List of Tables --- p.xii / Chapter Chapter 1: --- Introduction --- p.1 / Chapter 1.1 --- Alzheimer's Disease --- p.1 / Chapter 1.1.1 --- Cholinergic hypothesis --- p.2 / Chapter 1.1.2 --- p-amyloid hypothesis --- p.2 / Chapter 1.1.3 --- Taupathy hypothesis --- p.3 / Chapter 1.1.4 --- Current therapies --- p.4 / Chapter 1.2 --- Proteins Involved in Alzhemer's Disease --- p.5 / Chapter 1.2.1 --- Acetylcholinesterase (AChE) --- p.5 / Chapter 1.2.2 --- p-amyloid --- p.6 / Chapter 1.2.3 --- Paired helical filaments (PHF) --- p.7 / Chapter 1.2.4 --- Protein kinases --- p.8 / Chapter 1.2.4.1 --- Glycogen synthase kinase-3 (GSK-3) --- p.9 / Chapter 1.2.4.2 --- Cyclin-dependent kinase-5 (CDK-5) --- p.9 / Chapter 1.2.5 --- Protein phosphatase (PP) --- p.10 / Chapter 1.2.5.1 --- Protein phosphatase 1 (PP-1) --- p.11 / Chapter 1.2.5.2 --- Protein phosphatise 2A (PP-2A) --- p.12 / Chapter 1.2.5.3 --- Protein phosphatise 2B (PP-2B) --- p.13 / Chapter 1.2.6 --- Apoptotic and Anti-apoptotic proteins --- p.14 / Chapter 1.2.6.1 --- Caspase-3 --- p.15 / Chapter 1.2.6.2 --- Bcl-2 --- p.15 / Chapter 1.3 --- Flavonoids --- p.16 / Chapter 1.3.1 --- Biosynthesis of flavonoids --- p.17 / Chapter 1.3.2 --- Biological functions of flavonoids in plants --- p.18 / Chapter 1.3.3 --- Beneficial effects of flavonoids on human health --- p.19 / Chapter Chapter 2: --- Materials and Methods --- p.20 / Chapter 2.1 --- Differentiation of SHSY-5Y cells --- p.20 / Chapter 2.1.1 --- SHSY-5Y cell culture --- p.20 / Chapter 2.1.2 --- Counting cells --- p.20 / Chapter 2.1.3 --- Retinoic acid differentiation --- p.21 / Chapter 2.2 --- Western blot analysis --- p.21 / Chapter 2.2.1 --- Extraction of proteins from mammalian cells --- p.21 / Chapter 2.2.2 --- Sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) --- p.22 / Chapter 2.2.3 --- Semi-dry protein transfer to nitrocellulose membrane --- p.23 / Chapter 2.2.4. --- Membrane blocking and immunostaining --- p.24 / Chapter 2.3 --- MTT assay --- p.25 / Chapter 2.4 --- Hoechst 33342 Nuclei staining --- p.25 / Chapter 2.5 --- Cell cycle analysis --- p.25 / Chapter 2.5.1 --- Ethanol fixation --- p.25 / Chapter 2.5.2 --- Propidium iodide staining --- p.26 / Chapter 2.6 --- Annexin V-FITC & Propidium iodide staining --- p.26 / Chapter 2.7 --- DNA fragmentation analysis --- p.26 / Chapter 2.7.1 --- Phenol/Chloroform extraction of DNA --- p.26 / Chapter 2.7.2 --- Ethanol precipitation of DNA --- p.27 / Chapter 2.7.3 --- Agarose gel electrophoresis of DNA --- p.27 / Chapter 2.8 --- Proteomic analysis --- p.28 / Chapter 2.8.1 --- First dimension: isoelectric focusing --- p.28 / Chapter 2.8.2 --- Second dimension: SDS PAGE --- p.29 / Chapter 2.8.3 --- Gel staining --- p.30 / Chapter 2.8.3.1 --- Silver staining --- p.30 / Chapter 2.8.3.2 --- SYBRO Ruby staining --- p.31 / Chapter 2.8.4 --- Gel scanning and image analysis --- p.31 / Chapter 2.8.5 --- ln-gel digestion --- p.32 / Chapter 2.8.6 --- Zip Tip for desalting the digested sample --- p.33 / Chapter 2.8.7 --- Protein identification with mass spectrometry and database search --- p.33 / Chapter Chapter 3: --- Characterization of Okadaic acid-induced tail hyperphosphorylation in SHSY-5Y cells --- p.35 / Chapter 3.1 --- Introduction --- p.35 / Chapter 3.2 --- Objectives --- p.37 / Chapter 3.3 --- Results --- p.38 / Chapter 3.3.1 --- Differentiation of SH-SY5Y cell --- p.38 / Chapter 3.3.2 --- Changes of protein expression after okadaic acid treatment --- p.40 / Chapter 3.3.3 --- Neurite Retraction Induced by okadaic acid --- p.42 / Chapter 3.3.4 --- Okadaic acid-induced Cell Death measured by MTT assay --- p.44 / Chapter 3.3.5 --- Hoechst 33342 Nuclei Staining --- p.44 / Chapter 3.3.6 --- Cell cycle analysis by propidium iodide staining --- p.47 / Chapter 3.3.7 --- Early Apoptotic cells detection by Annexin V/PI staini --- p.49 / Chapter 3.3.8 --- DNA fragmentation --- p.51 / Chapter 3.4 --- Discussion --- p.53 / Chapter Chapter 4: --- Flavonoids screening for protecting neuronal death by preventing tau hyperphosphorylation --- p.57 / Chapter 4.1 --- Introduction --- p.57 / Chapter 4.2 --- Objectives --- p.58 / Chapter 4.3 --- Tested flavonoids --- p.59 / Chapter 4.4 --- Results --- p.60 / Chapter 4.4.1 --- Toxicity of flavonoids --- p.60 / Chapter 4.4.2 --- Effects of flavonoid pre-treatment on OA-induced neu retractions and cell death --- p.62 / Chapter 4.4.3 --- Western blot analysis --- p.65 / Chapter 4.4.4 --- The effect of different concentrations of hesperidin or OA treatment --- p.70 / Chapter 4.4.5 --- Proteomic analysis --- p.74 / Chapter 4.5 --- Discussion --- p.78 / Chapter Chapter 5: --- General Discussion --- p.82 / References