Please use this identifier to cite or link to this item: http://hdl.handle.net/20.500.12779/6261
Title: Antioxidants inhibit SAA formation and pro-inflammatory cytokine release in a human cell model of alkaptonuria.
Authors: Spreafico, Adriano
Millucci, Lia 
Ghezzi, Lorenzo
Geminiani, Michela 
Braconi, Daniela 
Amato, Loredana
Chellini, Federico
Frediani, Bruno
Moretti, Elena
Collodel, Giulia
Bernardini, Giulia 
Santucci, Annalisa 
Issue Date: 2013
Project: None 
Journal: RHEUMATOLOGY
Abstract: 
OBJECTIVE: Alkaptonuria (AKU) is an ultra-rare autosomal recessive disease that currently lacks an appropriate therapy. Recently we provided experimental evidence that AKU is a secondary serum amyloid A (SAA)-based amyloidosis. The aim of the present work was to evaluate the use of antioxidants to inhibit SAA amyloid and pro-inflammatory cytokine release in AKU.METHODS:We adopted a human chondrocytic cell AKU model to evaluate the anti-amyloid capacity of a set of antioxidants that had previously been shown to counteract ochronosis in a serum AKU model. Amyloid presence was evaluated by Congo red staining. Homogentisic acid-induced SAA production and pro-inflammatory cytokine release (overexpressed in AKU patients) were evaluated by ELISA and multiplex systems, respectively. Lipid peroxidation was evaluated by means of a fluorescence-based assay.RESULTS:Our AKU model allowed us to prove the efficacy of ascorbic acid combined with N-acetylcysteine, taurine, phytic acid and lipoic acid in significantly inhibiting SAA production, pro-inflammatory cytokine release and membrane lipid peroxidation.CONCLUSION:All the tested antioxidant compounds were able to reduce the production of amyloid and may be the basis for establishing new therapies for AKU amyloidosis.
Description: 
60006
URI: http://hdl.handle.net/20.500.12779/6261
ISSN: 1462-0324
DOI: 10.1093/rheumatology/ket185
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