pelargonidin-3-glucoside and Inflammation

The present study investigates the effect of strawberry antioxidants in beverage form on meal-induced postprandial inflammatory and insulin responses in human subjects. Overweight adults (n 24) consumed a high-carbohydrate, moderate-fat meal (HCFM) accompanied by either a strawberry or a placebo beverage in a cross-over design. Postprandial changes in plasma anthocyanins, their metabolites, insulin, glucose and inflammatory markers were assessed for 6 h. The postprandial concentrations of pelargonidin sulfate and pelargonidin-3-O-glucoside were significantly increased when the strawberry beverage was consumed concurrently with the HCFM compared with the placebo beverage (P < 0·001). The strawberry beverage significantly attenuated the postprandial inflammatory response as measured by high-sensitivity C-reactive protein and IL-6 (P < 0·05) induced by the HCFM. It was also associated with a reduction in postprandial insulin response (P < 0·05). Collectively, these data provide evidence for favourable effects of strawberry antioxidants on postprandial inflammation and insulin sensitivity.

Topics: Adult; Anthocyanins; Beverages; C-Reactive Protein; California; Cross-Over Studies; Female; Fragaria; Glucosides; Humans; Inflammation; Insulin; Interleukin-6; Male; Middle Aged; Oxidants; Oxidative Stress; Placebos; Postprandial Period; Single-Blind Method; Sulfates; Time Factors

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

Microglia are the major immune cells in the central nervous system. Microglial activation can be beneficial or detrimental depending on the stimuli and the physiopathological environment. Microglial activation is involved in a variety of neurodegenerative disorders. Different anesthetic agents have exhibited diverse effects on microglial activation and the engulfment process. The anthocyanin callistephin has been demonstrated to have antioxidant and anti‑inflammatory properties, and these were assessed in the present study, with a focus on its effect on microglial activation. Mouse microglial cells C8‑4B were treated with 100 ng/µl lipopolysaccharide (LPS) and 1 ng/µl interferon‑γ. Cells were subsequently treated with 2% isoflurane, 100 µM callistephin or both. LPS promoted apoptosis in C8‑B4 cells, and this was reduced following treatment with isoflurane and callistephin. LPS‑treated C8‑B4 cells also exhibited enhanced production of reactive oxygen species and nitric oxide, excessive engulfment and increased caspase 3/7 activity. These detrimental alterations were suppressed following co‑treatment with isoflurane and callistephin. LPS‑induced apoptosis was facilitated via the expression of B‑cell lymphoma‑2 like 1 and poly (ADP‑ribose) polymerase, which were subsequently restored following treatment with isoflurane and callistephin. Callistephin was demonstrated to be involved in the modulation of inducible nitric oxide synthase, cytochrome c oxidase subunit 2, tumor necrosis factor‑α and nuclear factor‑κ B. Callistephin enhanced the protective effects of isoflurane by modulating engulfment and apoptosis in C8‑B4 cells. The potential underlying mechanism was identified to be the suppression of p38 phosphorylation. The present study thus suggested that the negative effects on microglial activity induced by LPS were ameliorated following treatment with callistephin, which also enhanced the effects of isoflurane. Callistephin may therefore constitute a candidate drug agent that may target inflammatory and growth regulatory signaling pathways, thus ameliorating certain aspects of neurodegenerative diseases.

Topics: Animals; Anthocyanins; Anti-Inflammatory Agents; Antioxidants; Apoptosis; Cell Line; Inflammation; Isoflurane; Lipopolysaccharides; Mice; Microglia; Nitric Oxide; Phagocytosis; Reactive Oxygen Species