Anti-inflammatory activity of polyphenolics from açai (Euterpe oleracea Martius) in intestinal myofibroblasts CCD-18Co cells

Food Funct. 2015 Oct;6(10):3249-56. doi: 10.1039/c5fo00278h.

Abstract

The demand for tropical fruits high in polyphenolics including açai (Euterpe oleracea Mart.) has been increasing based on ascribed health benefits and antioxidant properties. This study evaluated the anti-inflammatory activities of açai polyphenolics in human colon myofibroblastic CCD-18Co cells to investigate the suppression of reactive oxygen species (ROS), and mRNA and protein expression of inflammatory proteins. Non-cytotoxic concentrations of açai extract, 1-5 mg gallic acid equivalent L(-1), were selected. The generation of ROS was induced by lipopolysaccharide (LPS) and açai extract partially reversed this effect to 0.53-fold of the LPS-control. Açai extract (5 mg GAE L(-1)) down-regulated LPS-induced mRNA-expression of tumor necrosis factor alpha, TNF-α (to 0.42-fold), cyclooxygenase 2, COX-2 (to 0.61-fold), toll-like receptor-4, TLR-4 (to 0.52-fold), TNF receptor-associated factor 6, TRAF-6 (to 0.64-fold), nuclear factor kappa-B, NF-κB (to 0.76-fold), vascular cell adhesion molecule 1, VCAM-1 (to 0.71-fold) and intercellular adhesion molecule 1, ICAM-1 (to 0.68-fold). The protein levels of COX-2, TLR-4, p-NF-κB and ICAM-1 were induced by LPS and the açai extract partially reversed this effect in a dose-dependent manner. These results suggest the anti-inflammatory effect of açai polyphenolic extract in intestinal cells are at least in part mediated through the inhibition of ROS and the expression of TLR-4 and NF-κB. Results indicate the potential for açai polyphenolics in the prevention of intestinal inflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Inflammatory Agents / pharmacology*
  • Antioxidants / pharmacology
  • Cell Line
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Down-Regulation
  • Euterpe / chemistry*
  • Gallic Acid / pharmacology
  • Humans
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / metabolism
  • Intestines / cytology*
  • Lipopolysaccharides / adverse effects
  • Myofibroblasts / cytology
  • Myofibroblasts / drug effects*
  • Myofibroblasts / metabolism
  • NF-kappa B / genetics
  • NF-kappa B / metabolism
  • Plant Extracts / pharmacology*
  • Polyphenols / pharmacology*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Reactive Oxygen Species / metabolism
  • TNF Receptor-Associated Factor 6 / genetics
  • TNF Receptor-Associated Factor 6 / metabolism
  • Toll-Like Receptor 4 / genetics
  • Toll-Like Receptor 4 / metabolism
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism
  • Vascular Cell Adhesion Molecule-1 / genetics
  • Vascular Cell Adhesion Molecule-1 / metabolism

Substances

  • Anti-Inflammatory Agents
  • Antioxidants
  • Lipopolysaccharides
  • NF-kappa B
  • Plant Extracts
  • Polyphenols
  • RNA, Messenger
  • Reactive Oxygen Species
  • TLR4 protein, human
  • TNF Receptor-Associated Factor 6
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1
  • Gallic Acid
  • Cyclooxygenase 2
  • PTGS2 protein, human