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Development of a New Model for the Induction of Chronic Kidney Disease via Intraperitoneal Adenine Administration, and the Effect of Treatment with Gum Acacia thereon
Author(s) -
Al Za'abi Mohammed,
Ali Badreldin,
Yasin Javed,
Schupp Nicole,
Nemmar Abderrahim
Publication year - 2015
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.29.1_supplement.938.3
Subject(s) - gum acacia , kidney disease , oral administration , oxidative stress , pharmacology , kidney , medicine , concomitant , chemistry , endocrinology , food science
Oral adenine (0.75% w/w in feed), is an established model for chronic kidney disease (CKD). Gum acacia (GA) has been shown to be a nephroprotective agent in this model. Here we aimed at developing an adenine‐induced CKD model in rats via a systemic route (intraperitoneal, i.p.) to test it with GA to obviate the possibility of a physical interaction between GA and adenine in the gut. Adenine was injected i.p. (50/100 mg/Kg for four weeks) and GA was given concomitantly in drinking water (15%, w/v). Several plasma and urinary biomarkers of oxidative stress were measured and renal damage was assessed histopathologically. Adenine, at the two given i.p. doses, significantly reduced body weight, and increased relative kidney weight, water intake and urine output. It dose‐dependently increased inflammatory and oxidative stress biomarkers, and caused morphological and histological damage resembling that which has been reported with oral adenine. Concomitant treatment with GA significantly mitigated almost all the above measured indices. Administration of adenine i.p. induced CKD signs very similar to those induced by oral adenine. Therefore, this model is quicker, more practical and accurate than the original (oral) model. GA ameliorates the CKD effects caused by adenine given i.p. suggesting that the antioxidant and anti‐inflammatory properties possessed by oral GA are the main mechanism for its salutary action in adenine‐induced CKD, an action that is independent of its possible interaction with adenine in the gut.