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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]

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]

Background: Increased platelet activity plays a significant role in the development of arterial thrombosis and cardiovascular disease (CVD). Natural antioxidants including anthocyanin (AC) have gained considerable interest due to their hypothesized antithrombotic potential.Primary Study Objective: Our study aimed to examine the in vitro effect of AC compounds on platelet activation and aggregation.Methods: Fasting blood samples were collected from healthy volunteers (n = 13). A full blood examination was done to exclude any abnormal specimen. Flow cytometer assessed platelet activity by recording platelet surface markers expression of P-selectin (CD62P) and PAC-1. Platelet aggregation studies were performed by stimulating platelets using three different agonists adenosine diphosphate (ADP), collagen and arachidonic acid (AA).Setting: The study was done in the school of Medical Sciences, Griffith University.Participants: Thirteen healthy adult participants were involved for blood collection.Intervention: AC was prepared using hemicellulose capsules sourced from Bilberries and Black Currants.Results: Anthocyanin (50 mg/L) significantly inhibited AA-induced platelet aggregation. Expression of P-selectin was significantly suppressed by 50 mg/L AC as measured by flow cytometer.Conclusions: AC attenuates platelet function by suppressing P-selectin expression and influencing Thromboxane A2 pathway (AA stimulation). These results provide further evidence for the effect of AC and the possible mechanism by which AC reduces platelet aggregation and activation. This study supports future human intervention trials to show that AC may act as a complement to other antiplatelet agents in reducing the risk of thrombosis. [ABSTRACT FROM AUTHOR]

Context • Type 2 diabetes mellitus is an independent precipitating factor for cardiovascular disease (CVD). Heart disease is one of the leading causes of mortality in patients with diabetes, mainly due to macrovascular complications, such as atherosclerosis. Although aspirin is a frequently used therapy for the inhibition of platelet hyperactivity, many studies suggest that aspirin resistance is rising. Objective • The study intended to investigate the benefits of anthocyanin (AC) as an antioxidant with inhibitory effects on platelets and, consequently, its potential usefulness as complementary antiplatelet therapy to attenuate the negative effects of atherosclerosis and CVD in patients with diabetes. Design • The research team performed a literature review. The team conducted a database search from 2007 to 2017 using Library of Congress, LISTA, PubMed, and Web of Science Core Collection databases, using the following keywords: anthocyanins, platelet, cardiovascular disease, and diabetes. Setting • The study took place at the School of Medical Sciences at Griffith University's Gold Coast campus (Southport, Australia). Results • Platelets have a major pathophysiological role of atherosclerosis and consequently CVD in diabetes. Antiplatelet drugs have a potent inhibitory effect of thrombotic and CVD risks in diabetes. Dietary antioxidants including ACs have a potential platelet inhibitory effect. Hence, ACs may act as complementary therapy to reduce CVD in diabetes. Conclusions • Although antiplatelet drugs such as aspirin provide significant action in the management of CVD, aspirin has limited benefits in diabetes. An AC antioxidant has a potential effect as an antiplatelet agent that subsequently can prevent atherosclerosis and CVD and, therefore, AC may be an alternative to other antiplatelet drugs such as aspirin. However, more interventional studies and large-scale clinical trials are necessary to prove the efficiency of AC as an alternative to other platelet-inhibitory drugs. [ABSTRACT FROM AUTHOR]