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Urinary metabolite profiling provides potential differentiation to explore the mechanisms of adjuvant‐induced arthritis in rats
Author(s) -
Jiang Hui,
Liu Jian,
Wang Ting,
Gao Jiarong,
Sun Yue,
Huang Chuanbing,
Meng Mei,
Qin Xiujuan
Publication year - 2016
Publication title -
biomedical chromatography
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.4
H-Index - 65
eISSN - 1099-0801
pISSN - 0269-3879
DOI - 10.1002/bmc.3697
Subject(s) - chemistry , metabolite profiling , metabolite , arthritis , urinary system , profiling (computer programming) , adjuvant , chromatography , pharmacology , computational biology , biochemistry , medicine , computer science , biology , operating system
To explore the pathogenesis of rheumatoid arthritis (RA) from the perspective of metabolomics, gas chromatography time‐of‐flight mass spectrometry (GC‐TOF/MS) technology was used to observe changes in the metabolic profiles of urine output from rats with adjuvant‐induced arthritis (AA). Sprague–Dawley rats were randomly divided into a control group and an experimental group, with eight in each. Rats in the experimental group were induced by intracutaneous innoculation of 0.1 mL Freund's complete adjuvant to right paws. On day 20 after immunization, the metabolic profiles between rat control and experimental groups were compared by combining GC‐TOF/MS technology with multivariate statistical approaches, including principal component analysis, partial least squares discriminant analysis and orthogonal projections to latent structures–discriminant analysis. Nine potential biomarkers were identified, including 2,2‐dimethylsuccinic acid, tartronic acid, dehydroshikimic acid, hippuric acid, adenine, phenaceturic acid, l ‐dopa, 1,4‐dihydroxy‐2‐naphthoic acid and melibiose. The findings indicate that the rats with AA are disturbed in metabolism of purine, amino acid, fat and energy. This study also demonstrates that the dysfunction in a range of biosynthetic and catabolic pathways, which leads to increased oxygen free radicals and inflammation, could cause underlying pathogenesis of RA. Copyright © 2016 John Wiley & Sons, Ltd.