Chemopreventive role of anthocyanins in atherosclerosis via activation of Nrf2-ARE as an indicator and modulator of redox

Biomed Pharmacother. 2015 May:72:30-6. doi: 10.1016/j.biopha.2015.03.008. Epub 2015 Apr 9.

Abstract

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.

Keywords: Anthocyanin; Atherosclerosis; Nrf2–Keap1; Oxidative stress.

Publication types

  • Review

MeSH terms

  • Animals
  • Anthocyanins / therapeutic use*
  • Antioxidant Response Elements / genetics*
  • Atherosclerosis / drug therapy*
  • Atherosclerosis / metabolism*
  • Chemoprevention*
  • Humans
  • NF-E2-Related Factor 2 / metabolism*
  • Oxidation-Reduction

Substances

  • Anthocyanins
  • NF-E2-Related Factor 2