cyanidin-3-o-beta-glucopyranoside has been researched along with delphinidin* in 5 studies
5 other study(ies) available for cyanidin-3-o-beta-glucopyranoside and delphinidin
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Anthocyanins, delphinidin-3-O-glucoside and cyanidin-3-O-glucoside, inhibit immune checkpoints in human colorectal cancer cells in vitro and in silico.
The objective was to assess anti-progression and stimulatory immune response effects among anthocyanins (ANC) and their metabolites on human colorectal cancer cells in vitro and in silico. Pure phenolics including delphinidin-3-O-glucoside (D3G) and its metabolites, delphinidin (DC) and gallic acid (GA), were tested alone or in combination, on HCT-116 and HT-29 human colorectal cancer cells (100-600 µg/mL). HCT-116 and HT-29 50% inhibition concentrations (µg/mL) were 396 ± 23 and 329 ± 17 for D3G; 242 ± 16 and >600 for DC; and 154 ± 5 and 81 ± 5 for GA, respectively. Using molecular docking, cyanidin-3-O-glucoside (C3G) showed the highest potential to inhibit immune checkpoints: programmed cell death protein-1 (PD-1) (-6.8 kcal/mol) and programmed death-ligand-1 (PD-L1) (-9.6 kcal/mol). C3G, D3G, DC, GA, and D3G-rich extracts decreased PD-L1 protein expression in HCT-116 cells. C3G decreased PD-L1 fluorescence intensity by 39%. ANC decreased PD-1 expression in peripheral blood mononuclear cells in monoculture by 41% and 55%, and co-culture with HCT-116 and HT-29 cells by 39% and 26% (C3G) and 50% and 51% (D3G), respectively. D3G and C3G, abundant in plant foods, showed potential for binding with and inhibiting immune checkpoints, PD-1 and PD-L1, which can activate immune response in the tumor microenvironment and induce cancer cell death. Topics: Adjuvants, Immunologic; Anthocyanins; Antineoplastic Agents, Immunological; Cell Survival; Colorectal Neoplasms; Glucosides; HCT116 Cells; HT29 Cells; Humans; Tumor Microenvironment | 2019 |
Anthocyanins and phenolic acids from a wild blueberry (Vaccinium angustifolium) powder counteract lipid accumulation in THP-1-derived macrophages.
Blueberries are a rich source of anthocyanins (ACNs) and phenolic acids (PA), which are hypothesized to protect against development of atherosclerosis. The present study examined the effect of an ACN- and PA-rich fractions, obtained from a wild blueberry powder, on the capacity to counteract lipid accumulation in macrophages derived from monocytic THP-1 cells. In addition, we tested the capacity of pure ACNs and their metabolites to alter lipid accumulation.. THP-1-derived macrophages were incubated with fatty acids (500 μM oleic/palmitic acid, 2:1 ratio) and different concentrations (from 0.05 to 10 μg mL(-1)) of ACN- and PA-rich fractions, pure ACN standards (malvidin, delphinidin and cyanidin 3-glucoside), and metabolites (syringic, gallic and protocatechuic acids). Lipid accumulation was quantified with the fluorescent dye Nile red.. Lipid accumulation was reduced at all concentrations of the ACN-rich fraction tested with a maximum reduction at 10 μg mL(-1) (-27.4%; p < 0.0001). The PA-rich fraction significantly reduced the lipid accumulation only at the low concentrations from 0.05 µg mL(-1) to 0.3 µg mL(-1), with respect to the control with fatty acids. Supplementation with pure ACN compounds (malvidin and delphinidin-3-glucoside and its metabolic products (syringic and gallic acid)) reduced lipid accumulation especially at the low concentrations, while no significant effect was observed after cyanidin-3-glucoside and protocatechuic acid supplementation.. The results demonstrated a potential role of both the ACN- and PA-rich fractions and single compounds in the lipid accumulation also at concentrations close to that achievable in vivo. Topics: Anthocyanins; Antioxidants; Atherosclerosis; Blueberry Plants; Carotenoids; Cell Line, Tumor; Cell Survival; Dietary Fiber; Dietary Sucrose; Fatty Acids; Gallic Acid; Glucosides; Humans; Hydroxybenzoates; Lipid Metabolism; Macrophages; Plant Extracts; Powders; Protective Agents; Trace Elements; Vitamins | 2016 |
Whole body radioprotective effect of phenolic extracts from the fruits of Malus baccata (Linn.) Borkh.
This study was designed to evaluate the radioprotective effect of phenolics extracted from the fruits of Malus baccata (Linn.) Borkh. (MBP-3b) against damage induced by (60)Co γ-irradiation in vivo. MBP-3b could significantly improve the activity of endogenous antioxidant enzymes and the T-AOC, as well as reduce the MDA level in the liver and kidneys of irradiated mice. In addition, pretreatment with MBP-3b at a dose of 150 mg per kg bw could significantly enhance immunomodulation activity by promoting the proliferation of spenocytes and monocyte phagocytosis. The administration of MBP-3b prevented the decline induced by radiation of haematological parameters (WBC, RBC, PLT and HGB). Furthermore, MBP-3b could protect spenocytes from radiation-induced damage by inhibiting cell apoptosis. The results indicated that MBP-3b possesses strong whole body radioprotective and immunomodulatory activities. The main constituents of MBP-3b were tentatively identified as delphinidin-3,5-diglucoside, cyanidin-3-glucoside, chlorogenic acid, proanthocyanidin C1, quercetin-3-galactoside, quercetin-3-glucoside, quercetin-3-xyloside/arabinoside, phloretin-2-xyloseglucoside, quercetin-3-rhamnoside and phlorizin. MBP-3b could be used as a probable radioprotector against gamma radiation induced oxidative damage. Topics: Animals; Anthocyanins; Antioxidants; Apoptosis; Cell Proliferation; Chlorogenic Acid; Fruit; Gamma Rays; Glucosides; Male; Malondialdehyde; Malus; Mice; Phenols; Plant Extracts; Proanthocyanidins; Quercetin; Radiation-Protective Agents; Spleen | 2016 |
Phenolic Compounds from Fermented Berry Beverages Modulated Gene and Protein Expression To Increase Insulin Secretion from Pancreatic β-Cells in Vitro.
Berries are a rich source of bioactive phenolic compounds that are able to bind and inhibit the enzyme dipeptidyl peptidase-IV (DPP-IV), a current target for type-2 diabetes therapy. The objectives were to determine the role of berry phenolic compounds to modulate incretin-cleaving DPP-IV and its substrate glucagon-like peptide-1 (GLP-1), insulin secretion from pancreatic β-cells, and genes and proteins involved in the insulin secretion pathway using cell culture. Anthocyanins (ANC) from 50% blueberry-50% blackberry (Blu-Bla) and 100% blackberry (Bla) fermented beverages at 50 μM cyanidin-3-glucoside equivalents increased (p < 0.05) glucose-stimulated insulin secretion from pancreatic β-cells (iNS-1E) both when applied directly and following simulated absorption through Caco-2 cells (by 233 and 100 μIU insulin/mL, respectively). ANC 50%Blu-Bla and ANC 100%Bla upregulated the gene for incretin hormone GLP-1 (fold-change 3.0 ± 1.4 and 2.0 ± 0.3, respectively) and genes in the insulin secretory pathway including insulin-like growth factor 1 receptor (iGF1R, 2.3 ± 0.6 and 1.6 ± 0.3, respectively), and increased (p < 0.05) the protein expression of insulin-like growth factor 2 (IGF-II), insulin-like growth factor binding proteins (IGFBP-2 and 3), and vascular endothelial growth factor (VEGF) in iNS-1E cells. Taken together, anthocyanins, predominantly delphinidin-3-arabinoside, from fermented berry beverages have the potential to modulate DPP-IV and its substrate GLP-1, to increase insulin secretion, and to upregulate expression of mRNA of insulin-receptor associated genes and proteins in pancreatic β-cells. Topics: Anthocyanins; Beverages; Blood Glucose; Caco-2 Cells; Dipeptidyl Peptidase 4; Dipeptidyl-Peptidase IV Inhibitors; Fermentation; Fruit; Gastric Inhibitory Polypeptide; Glucagon-Like Peptide 1; Glucosides; Humans; Hypoglycemic Agents; Insulin; Insulin-Like Growth Factor Binding Protein 2; Insulin-Secreting Cells; Phenols; Vascular Endothelial Growth Factor A | 2016 |
Blockade of the renin-angiotensin system with delphinidin, cyanin, and quercetin.
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 | 2012 |