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The purpose of the study was to assess the effects of anthocyanin-rich Queen Garnet plum juice (QGPJ) on body weight and expression of leptin and adiponectin. Queen Garnet plum is a Japanese plum ( Prunus salicina ) cultivar developed through a Queensland Government breeding program with very high levels of anthocyanins (272 mg/100 g). Twenty healthy volunteers were supplemented with 200 ml/day of QGPJ and placebo drink for 4 weeks. Supplementation with QGPJ significantly reduces body weight and BMI ( p  < 0.05) with the average decrease of 0.6 kg in body weight and 0.2 units in BMI over the period of 4 weeks. Furthermore, consumption of QGPJ significantly increases adiponectin blood levels ( p  < 0.05) (average increase of 3.83 µg/mL) and decreases leptin blood levels (average decrease of 1.31 ng/mL). QGPJ may have potential to be used as a functional food for preventing obesity and obesity related disorders. [ABSTRACT FROM AUTHOR]

Anthocyanins have been reported to induce the expression of enzymes involved in both cellular antioxidant defenses and attenuating inflammation-associated pathogenesis. Induction of such enzymes by edible anthocyanin largely accounts for their atherosclerosis chemo-protective activities. Nuclear factor erythroid 2-related factor 2 (Nrf2) plays an essential role in the coordinated induction of those genes encoding redox-responsive and cellular defense antioxidant enzyme termed antioxidant response element (ARE). Current studies have revealed that Nrf2–ARE signaling is involved in attenuating inflammation-associated pathogenesis such as atherosclerosis. Conversely, reduction in Nrf2 signaling leads to enhanced susceptibility to oxidative stress and inflammatory tissue injuries. The activation of Nrf2–ARE might inhibit the production of pro-inflammatory mediator including cyclooxygenase-2, chemokines, cytokines, cell adhesion molecules, and induction nitric oxide synthase. This review highlights the gene expression induced by dietary anthocyanin via Nrf2 signaling on redox-regulated transcription factor in atherosclerosis disorders. [ABSTRACT FROM AUTHOR]

Increased oxidant production in humans induces a number of thrombotic consequences; including platelet hyperactivity/aggregability, which could be countered through specifically developed functional foods. We sought to determine the antithrombotic properties of anthocyanin-rich Queen Garnet plum juice (QGPJ) supplementation with and without exercise-induced oxidative stress. Thirteen healthy participants were investigated in a randomised, double-blind, placebo-controlled, cross-over trial. Participants consumed 200 mL/day of QGPJ and placebo juice for 28-days, with treatments separated by a two-week wash-out period. Blood samples were collected at baseline and after 1 h of exercise (70% peak-O 2 uptake) both before and after oral supplementation and evaluated for platelet function and haemostatic activity. QGPJ supplementation inhibited adenosine diphosphate-induced platelet aggregation both without and under exercise-induced oxidative stress by 10.7% (P < 0.01) and 12.7% (P < 0.001) respectively; arachidonic acid-induced aggregation under oxidative stress by 28.8% (P < 0.05); reduced platelet activation-dependant P-selectin expression by 32.9% (P < 0.01) and 38.7% (P < 0.001) both without and under oxidative stress respectively; and exhibited favourable effects on coagulation parameters both with and without oxidative stress. The anti-thrombotic activity exhibited by anthocyanin-rich QGPJ suggests a potential for cardiovascular disease risk reduction and may be considered as complementary anti-platelet nutritional therapy in pro-thrombotic population. [ABSTRACT FROM AUTHOR]

The anti-thrombotic properties of an anthocyanin-rich Queen Garnet plum juice (QGPJ) and anthocyanin-free prune juice (PJ) were studied in this randomised, double-blind, crossover trial. Twenty-one healthy subjects (M = 10, F = 11) consumed QGPJ, PJ or placebo, 200 mL/day for 28-days followed by a 2-week wash-out period. Only QGPJ supplementation inhibited platelet aggregation induced by ADP (<5%, P  = 0.02), collagen (<2.7%, P  < 0.001) and arachidonic acid (<4%, P  < 0.001); reduced platelet activation-dependent surface-marker P-selectin expression of activated de-granulated platelets (<17.2%, P  = 0.04); prolonged activated-partial thromboplastin clotting time (>2.1 s, P  = 0.03); reduced plasma-fibrinogen (<7.5%, P  = 0.02) and malondialdehyde levels, a plasma biomarker of oxidative stress ( P  = 0.016). PJ supplementation increased plasma hippuric acid content ( P  = 0.018). QGPJ or PJ supplementation did not affect blood cell counts, lipid profile, or inflammation markers. Our findings suggest that QGPJ but not PJ has the potential to significantly attenuate thrombosis by reducing platelet activation/hyper-coagulability and oxidative stress. [ABSTRACT FROM AUTHOR]

Type 2 diabetes is associated with oxidative stress and low-grade inflammation resulting in endothelial dysfunction (ED). This study determined to explore the protective effects of berry-derived anthocyanins (AC) with potent antioxidant and anti-inflammatory activities in human diabetic endothelial cells upon oxidative and inflammatory stressors. Cultured healthy human aortic endothelial cells (HAEC) and diabetic human aortic endothelial cells (D-HAEC) exposed to oxidative stress by hydrogen peroxide (H 2 O 2 , 75 μM) and lipopolysaccharide (LPS, 1 μg/mL) as an inflammatory inducer before treatment with AC (50 μl/ml). The results from cytotoxicity assays showed that AC had no significant effects in cell viability (P-value < 0.0001), and exposure to H 2 O 2 75 μM had a less toxic effect (P-value < 0.05). Although, AC significantly decreased H 2 O 2 -induced cytotoxicity and oxidative stress in both HAEC and D-HAEC cell lines (P-value < 0.0001), no positive impact of AC was found on the GSSG/GSH ratios (P-value < 0.05). Exposure to the LPS increased the production of IL-6 in both HAEC and D-HAEC cell lines (P-value < 0.0001), whereas AC treatment reduced LPS‐induced IL‐6 production in both cell lines with a more robust impact on D-HAEC (P-value < 0.0001). While LPS increased inflammasome assembling and caspase-1 activation, AC treatment inhibited caspase-1 activation in D-HAEC (P ≤ 0.05). This study indicated that berry anthocyanins reduced oxidative stress and inflammation via the inhibition of the NF-ƙB signaling pathway, which contributes to mitigating the diabetes-induced up-regulation of NF-ƙB. • T2DM is associated with oxidative stress and inflammation resulting in ED. • Anthocyanins (AC) decreased H 2 O 2 -induced cytotoxicity in both HAEC & D-HAEC. • AC reduced LPS‐induced IL‐6 production in the diabetic endothelial cell line. • AC treatment inhibited LPS‐induced caspase-1 activation in D-HEAC. • AC protected D-HAECs via anti-inflammatory mechanisms to prevent diabetic ED. [ABSTRACT FROM AUTHOR]

• Anthocyanin's anti-inflammatory properties were investigated. • ACN supplementation significantly decreases blood plasma levels of CCL2. • ACN supplementation significantly decreases blood plasma levels of IL-6. • ACN displays potential as a complementary anti-inflammatory therapeutic agent. Chronic low-grade inflammation in obese and overweight individuals is associated with an increased risk of type II diabetes and cardiovascular disease. The current trial investigated the anti-inflammatory properties of anthocyanin (ACN) supplementation in lean, overweight and obese individuals. Fifteen lean, ten overweight and ten obese participants consumed ACN (320 mg/day) for 28 days along with their usual diet. ACN supplementation significantly decreased blood plasma levels of CCL2 in the lean, overweight and obese groups (p < 0.0001, p < 0.0001 and p < 0.01 respectively). Additionally, significantly decreased levels of IL-6 in the obese group (p < 0.05) were also observed post-ACN supplementation. In conclusion, these results demonstrate the anti-inflammatory potential of ACN and suggest the supplementation of ACN as a complementary therapeutic agent for reducing chronic inflammation in obese and overweight individuals. [ABSTRACT FROM AUTHOR]