impact factor
logo
 

Full Papers

 

Components of tart cherry juice inhibit NFκB activation and inflammation in acute gout


1, 2, 3, 4, 5, 6

 

  1. Rutgers Robert Wood Johnson Medical School, Gout Center and Division of Rheumatology, Department of Medicine, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ, USA. schlesna@rwjms.rutgers.edu
  2. AMPEL BioSolutions, Charlottesville, VA, USA.
  3. Division of Immunology and Rheumatology, Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
  4. Division of Immunology and Rheumatology, Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
  5. Ernest Mario School of Pharmacy, Piscataway, NJ, USA.
  6. Division of Immunology and Rheumatology, Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.

CER14734
Full Papers

purchase article

PMID: 34369352 [PubMed]

Received: 19/04/2021
Accepted : 09/07/2021
In Press: 24/07/2021

Abstract

OBJECTIVES:
To identify the anthocyanin content in tart cherry juice concentrate (TCJC) and establish the anti-inflammatory effect of in a murine acute gout model.
METHODS:
The main anthocyanins in the TCJC were identified by liquid chromatography mass spectroscopy (LCMS). TCJC or phosphate-buffered saline (PBS) as control were administered daily by oral gavage to BALB/C-Tg(NFκB-RE-luc)-Xen mice that harbour a firefly luciferase cDNA reporter under the regulation of 3 Nuclear factor-κB (NF-κB) response elements. After 14 days, gouty inflammation was induced by intra-articular injection of monosodium urate (MSU) crystals into the tibio-tarsal joint (ankle). NF-κB activity was measured locally in the injected ankle using the Xenogen in vivo imaging system (IVIS), and decalcified feet/ankles were paraffin-embedded and analysed histopathologically.
RESULTS:
The major anthocyanin compound present in TCJC was cyanidin 3-glucosylrutinoside followed by cyanidin 3-rutinoside. In the murine acute gout model, MSU injection increased NF-κB activity and oral administration of TCJC significantly reduced NF-κB activity in mouse foot, and ankle joints as assessed by IVIS analysis. Bioluminescent imaging detection of NF-κB activation was inhibited approximately 2-fold relative to control mice receiving PBS. Histopathologic examination showed suppression of infiltrates into the tibio-tarsal joint space of the mice receiving TCJC compared to PBS-treated control counterparts.
CONCLUSIONS:
The major anthocyanin in TCJC was cyanidin 3-glucosylrutinoside. Clinically relevant doses of TCJC significantly inhibit inflammation and NF-κB activation induced by MSU crystals.

Rheumatology Article