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Effect of gum Arabic on oxidative stress and inflammation in adenine–induced chronic renal failure in rats
Author(s) -
Ali Badreldin H.,
Al-Husseni Isehaq,
Beegam Sumyia,
Al Shukali Ahmed A.,
Nemmar Abderrahim,
Schupp Nicole
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1051.9
Subject(s) - creatinine , oxidative stress , inflammation , endocrinology , renal function , medicine , urine , kidney , kidney disease , chemistry , pathogenesis
Inflammation and oxidative stress are known to be involved in the pathogenesis of chronic kidney disease in humans, and in surgically‐induced chronic renal failure (CRF) in rats. Evidence for the involvement of these processes in adenine‐induced CRF in rats is lacking. The aim of this work was to study the role of inflammation and oxidative stress in adenine‐induced CRF, and the effect thereon of the purported nephroprotective agent gum arabic (GA). Rats were divided into four groups and treated for 4 weeks as follows: control, adenine in the feed (0.75%, w/w), GA in drinking water (15%,w/v) and adenine + GA, as before. Urine, blood and kidneys were collected from the rats at the end of the treatment for analysis of conventional renal function tests (plasma creatinine and urea concentration and urinary NAG activity). In addition, the concentrations of several pro‐inflammatory cytokines and indices of oxidative stress, renal apoptosis, superoxide formation and DNA double strand break frequency detected with immunohistochemistry for γ‐H2AX were also conducted in the kidney tissue, plasma and urine. Adenine (0.75% in the feed for 4 weeks) caused significant increases ( P < 0.001) in the concentrations of urea and creatinine in plasma, significantly decreased the creatinine clearance ( P < 0.01) and induced significant increases in the concentration of the measured inflammatory mediators. Treatment with GA significantly ameliorated these actions, suggesting that the mechanism of the reported salutary effect of GA in adenine‐induced CRF is associated with mitigation of the adenine‐induced inflammation and generation of free radicals.

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