pelargonidin-3-glucoside and peonidin-3-glucoside

Formation of advanced glycation end products (AGEs), which are associated with diabetes mellitus, contributes to prominent features of osteoarthritis, i.e., inflammation-mediated destruction of articular cartilage. Among the phytochemicals which play a role in anti-inflammatory effects, anthocyanins have also been demonstrated to have anti-diabetic properties. Purple corn is a source of three major anthocyanins: cyanidin-3-O-glucoside, pelargonidin-3-O-glucoside and peonidin-3-O-glucoside. Purple corn anthocyanins have been demonstrated to be involved in the reduction of diabetes-associated inflammation, suggesting that they may have a beneficial effect on diabetes-mediated inflammation of cartilage. This investigation of the chondroprotective effects of purple corn extract on cartilage degradation found a reduction in glycosaminoglycans released from AGEs induced cartilage explants, corresponding with diminishing of uronic acid loss of the cartilage matrix. Investigation of the molecular mechanisms in human articular chondrocytes showed the anti-inflammatory effect of purple corn anthocyanins and the metabolite, protocatechuic acid (PCA) on AGEs induced human articular chondrocytes via inactivation of the NFκb and MAPK signaling pathways. This finding suggests that purple corn anthocyanins and PCA may help ameliorate AGEs mediated inflammation and diabetes-mediated cartilage degradation.

Topics: Anthocyanins; Cartilage; Cell Line; Chondrocytes; Diabetes Complications; Diabetes Mellitus; Glucosides; Glycation End Products, Advanced; Glycosaminoglycans; Humans; Hydroxybenzoates; Inflammation; MAP Kinase Signaling System; NF-kappa B; Osteoarthritis; Zea mays

This study aimed to investigate the associations between phenolic composition of selected purple maize genotypes and their anti-inflammatory, anti-adipogenic and anti-diabetic properties in vitro. Anthocyanin-rich water extracts (PMWs) from 20 purple maize genotypes were evaluated in RAW 264.7 macrophages and 3T3-L1 adipocytes under different conditions. Cyanidin-3-O-glucoside (C3G), pelargonidin-3-O-glucoside (Pr3G), peonidin-3-O-glucoside (P3G) and corresponding acylated forms were major anthocyanins in PMW, accompanied by ten tentatively identified non-anthocyanin phenolics. Correlation studies showed that C3G, P3G, and derivatives, but not Pr3G and its acylated form contributed to the biological properties of PMW. Besides anthocyanins, quercetin, luteolin, and rutin were the dominant anti-inflammatory and anti-diabetic components, in terms of down-regulating pro-inflammatory mediator production in inflamed macrophages and adipocytes, modulating diabetes-related key enzymes and improving insulin sensitivity in insulin-resistant adipocytes. Quercetin and phenolic acids, especially vanillic acid and protocatechuic acid, were closely associated with anti-adipogenic properties of PMW via inhibition of the preadipocyte-adipocyte transition.

Topics: 3T3-L1 Cells; Adipocytes; Adipogenesis; Animals; Anthocyanins; Anti-Inflammatory Agents; Cell Differentiation; Genotype; Glucosides; Hypoglycemic Agents; Insulin Resistance; Mice; Phenols; Plant Extracts; Principal Component Analysis; RAW 264.7 Cells; Reactive Oxygen Species; Tumor Necrosis Factor-alpha; Zea mays

Anthocyanins have been studied as potential antimicrobial agents against Helicobacter pylori. We investigated whether the biosynthesis and secretion of cytotoxin-associated protein A (CagA) and vacuolating cytotoxin A (VacA) could be suppressed by anthocyanin treatment in vitro. H. pylori reference strain 60190 (CagA(+)/VacA(+)) was used in this study to investigate the inhibitory effects of anthocyanins; cyanidin 3-O-glucoside (C3G), peonidin 3-O-glucoside (Peo3G), pelargonidin 3-O-glucoside (Pel3G), and malvidin 3-O-glucoside (M3G) on expression and secretion of H. pylori toxins. Anthocyanins were added to bacterial cultures and Western blotting was used to determine secretion of CagA and VacA. Among them, we found that C3G inhibited secretion of CagA and VacA resulting in intracellular accumulation of CagA and VacA. C3G had no effect on cagA and vacA expression but suppressed secA transcription. As SecA is involved in translocation of bacterial proteins, the down-regulation of secA expression by C3G offers a mechanistic explanation for the inhibition of toxin secretion. To our knowledge, this is the first report suggesting that C3G inhibits secretion of the H. pylori toxins CagA and VacA via suppression of secA transcription.

Topics: Anthocyanins; Antigens, Bacterial; Bacterial Proteins; Gene Expression Regulation, Bacterial; Glucosides; Helicobacter pylori; Humans