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Metabolic syndrome (MetS) is a global challenge for atherosclerosis. It was hypothesized that a four-week consumption of anthocyanin supplements by MetS patients who had three or more risk factors linked with metabolic syndrome would have a greater improvement in cardiometabolic biomarkers and would also reduce the risk of thrombosis. A total of 55 participants in two groups of Normal healthy and MetS (age 25-75y) were given 320 mg anthocyanin supplements twice daily for 4 weeks. Platelet coagulant activities, lipid profiles, fasting blood glucose, and inflammatory and oxidative stress biomarkers were measured before and after supplementation to evaluate the atheroprotective effects of anthocyanins in the study subjects. Four weeks of anthocyanin supplementation significantly decreased cardiometabolic risk factors including the average serum fasting blood glucose (FBG) (by 13.3%, P < .05) and lipid profiles by significant reduction in triglyceride (by 24.9%, P < .05) and LDL-C (by 33.1%, P < .05) in the MetS group. Anthocyanin supplementation also decreased high sensitivity C-reactive protein (hs-CRP) level (by 28%, P < .05) in females. However, no significant differences in serum UA (uric acid) and HDL-C were observed between anthocyanin pre- and post-treatment in both groups. Moreover, Anthocyanin supplements decreased ADP-induced platelet activation configuration expressed as P-selectin by 40% (P < .05). There was a positive correlation between decreased hs-CRP values and the levels of LDL-C and FBG in the MetS group (P < .05). These results support the hypothesis that anthocyanin supplementation exerts anti-atherogenicity effects by improving cardiometabolic risk factors and reducing thrombogenicity in the MetS population., (Copyright © 2020 Elsevier Inc. All rights reserved.)

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., (Copyright © 2015 Elsevier Masson SAS. All rights reserved.)