cyanidin-3-o-beta-glucopyranoside and Hypertension

Immune system dysfunction may contribute to the pathogenesis of hypertension in spontaneously hypertensive rats (SHR). We examined the effects of the anthocyanin, cyanidin 3-O-glucoside (C3G), and the diuretic, hydrochlorothiazide (HCT), on T-cell function in SHR. Five-week-old male SHR and Wistar-Kyoto (WKY) rats received water (n = 8/SHR; n = 8/WKY), 10 mg kg-1 day-1 C3G (n = 8/SHR; n = 8/WKY), 10 mg kg-1 day-1 HCT (n = 8/SHR; n = 8/WKY), or 10 mg kg-1 day-1 C3G + 10 mg kg-1 day-1 HCT (n = 8/SHR; n = 8/WKY) by oral gavage for 15 weeks. Spleens were used to assess T-cell phenotypes via flow cytometry and concanavalin A stimulated ex vivo cytokine production (IL-2, IL-10, TNFα, IFNγ) using a cytometric bead array. SHR had lower proportions of helper T-cells (Th) that were T-regulatory, CD62Llo, CD62L- and CD25+ compared to WKY. C3G treated SHR had higher proportions of Th that were CD62Llo and CD62L-, while HCT treated rats had higher CD62Lhi and CD62Llo and lower CD62L- compared to SHR control. The proportion of T-regulatory and Th that were CD25+ were not affected by treatment in SHR. Stimulated splenocytes from SHR produced lower concentrations of cytokines compared to WKY. C3G treated SHR produced higher while HCT treated SHR produced lower TNFα and IFNγ concentrations compared to controls. Our findings suggest that C3G has positive effects, whereas HCT further suppresses T-cell function in SHR.

Topics: Animals; Anthocyanins; Cytokines; Hydrochlorothiazide; Hypertension; Immunologic Memory; Immunophenotyping; Lymphocyte Activation; Lymphocyte Count; Male; Organ Size; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Spleen; T-Lymphocyte Subsets; T-Lymphocytes, Helper-Inducer; T-Lymphocytes, Regulatory

Increased consumption of dark-coloured fruits and vegetables may mitigate metabolic syndrome. This study has determined the changes in metabolic parameters, and in cardiovascular and liver structure and function, following chronic administration of either cyanidin 3-glucoside (CG) or Queen Garnet plum juice (QG) containing cyanidin glycosides to rats fed either a corn starch (C) or a high-carbohydrate, high-fat (H) diet. Eight to nine-week-old male Wistar rats were randomly divided into six groups for 16-week feeding with C, C with CG or QG, H or H with CG or QG. C or H were supplemented with CG or QG at a dose of ∼ 8 mg/kg/day cyanidin glycosides from week 8 to 16. H rats developed signs of metabolic syndrome including visceral adiposity, impaired glucose tolerance, hypertension, cardiovascular remodelling, increased collagen deposition in left ventricle, non-alcoholic fatty liver disease, increased plasma liver enzymes and increased inflammatory cell infiltration in the heart and liver. Both CG and QG reversed these cardiovascular, liver and metabolic signs. However, no intact anthocyanins or common methylated/conjugated metabolites could be detected in the plasma samples and plasma hippuric acid concentrations were unchanged. Our results suggest CG is the most likely mediator of the responses to QG but that further investigation of the pharmacokinetics of oral CG in rats is required.

Topics: Animals; Anthocyanins; Cardiovascular System; Diet, High-Fat; Dietary Carbohydrates; Dietary Fats; Dietary Supplements; Fruit and Vegetable Juices; Glucosides; Hypertension; Liver; Male; Metabolic Syndrome; Non-alcoholic Fatty Liver Disease; Prunus domestica; Rats; Rats, Wistar

Overactivation of the renin-angiotensin system is one of the most important risk factors for the development of hypertension. The use of the crude extracts and/or active compounds, such as anthocyanins and quercetin, of herbal plants that have antihypertensive effects is beneficial for decreasing of blood pressure level. However, the molecular mechanisms by which anthocyanins (delphinidin and cyanin) and quercetin regulate the renin-angiotensin system are not completely understood. In this study, we demonstrate that delphinidin, cyanin, and quercetin interrupt the renin-angiotensin system signaling pathway by inhibiting the angiotensin-converting enzyme activity and decreasing its mRNA production. Furthermore, treatment with either delphinidin or cyanin significantly inhibited renin mRNA production. However, delphinidin, cyanin, and quercetin did not act as the angiotensin II type 1 receptor antagonist and did not play roles in the regulation of its internalization. The direct inhibition of components of the renin-angiotensin system advances our understanding of the antihypertensive effects of these compounds.

Topics: Angiotensin-Converting Enzyme Inhibitors; Anthocyanins; Antihypertensive Agents; Blood Pressure; Glucosides; HEK293 Cells; Humans; Hypertension; Quercetin; Renin; Renin-Angiotensin System; Signal Transduction