4.7 Article

Anthocyanins reduce inflammation and improve glucose and lipid metabolism associated with inhibiting nuclear factor-kappaB activation and increasing PPAR-gamma gene expression in metabolic syndrome subjects

Journal

FREE RADICAL BIOLOGY AND MEDICINE
Volume 150, Issue -, Pages 30-39

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2020.02.004

Keywords

Anthocyanin; Metabolic syndrome; NF-kB; Nrf2; PPAR-gamma

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Anthocyanins exhibit antioxidant and anti-inflammatory activities via a multitude of biochemical mechanisms. However, the signaling pathways involved in the actions of anthocyanins against chronic inflammation are not fully understood. The effects of berry-rich anthocyanin supplements (320 mg/day) for four weeks were examined on features of metabolic syndrome components and the expression of PPAR-gamma, Nrf2, and NF-kappa B dependent genes in MetS and healthy subjects. Total RNA was isolated from whole blood with the PAXgene proprietary blood collection system. Four weeks anthocyanin consumption significantly decreased fasting blood glucose (15.7% vs 3.2%), TG (18.2% vs -1.39%), cholesterol (33.5% vs 1.56%) and LDL (28.4% vs -15.6%) in the MetS compared to Control group (P-value < 0.05, 95% CI). There was a significant up regulation in the expression PPAR-gamma gene associated with the lipid and glucose metabolism in MetS subjects which negatively correlated (P-value < 0.01) with the change in the FBG (r = -0.488), Cholesterol (r = -0.496), TG (r = -0.513) and LDL (r = -0.519). Moreover, anthocyanin supplementation decreases serum hs-CRP (-36.3% vs 6.25%) in MetS in compared to Control group (P-value < 0.05). Anthocyanin supplementation also down-regulated the expression of NF-kappa B dependent genes including TNF-alpha (-28% and -15%), IL-6 (-16.1% and -13.6%), IL-1A (-21.5% and -12.9%), PCAM-1 (-15% and -17.5%), and COX-2(-26% and -27%) in both MetS and Control group respectively (P-value < 0.05). The study results suggested that berry supplements improved selected features of metabolic syndrome and related cardiovascular risk factors. These benefits may be due to the inhibition of NF-kappa B dependent gene expression and enhancement of PPAR-gamma.

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