Full Papers
Components of tart cherry juice inhibit NFκB activation and inflammation in acute gout
N. Schlesinger1, P.E. Lipsky2, K. Jablonski3, W. Jarjour4, L. Brunetti5, N.A. Young6
- 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
- AMPEL BioSolutions, Charlottesville, VA, USA.
- Division of Immunology and Rheumatology, Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
- Division of Immunology and Rheumatology, Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
- Ernest Mario School of Pharmacy, Piscataway, NJ, USA.
- Division of Immunology and Rheumatology, Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
CER14734
2022 Vol.40, N°7
PI 1293, PF 1298
Full Papers
PMID: 34369352 [PubMed]
Received: 19/04/2021
Accepted : 09/07/2021
In Press: 24/07/2021
Published: 04/07/2022
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.
