PMID- 28302561 OWN - NLM STAT- MEDLINE DCOM- 20170428 LR - 20220310 IS - 1879-0631 (Electronic) IS - 0024-3205 (Linking) VI - 176 DP - 2017 May 1 TI - Ameliorative effect of gossypin against gentamicin-induced nephrotoxicity in rats. PG - 75-81 LID - S0024-3205(17)30092-9 [pii] LID - 10.1016/j.lfs.2017.03.009 [doi] AB - AIM: Gentamicin (GEN) is an aminoglycoside antibiotic employed in treatment of life-threatening gram-negative infections, but one of its major side effects is the induction of nephrotoxicity. Therefore, the aim of this work was to scrutinize the possible protective effect of gossypin against GEN-induced nephrotoxicity. METHOD: Rats were randomly divided into four groups. First group served as a control, second group was injected with gossypin (10mg/kg, orally) for 7days, third group was injected with GEN (80mg/kg, i.p.) and the fourth group was co-treated with GEN and gossypin for 7days. KEY FINDING: GEN-treated group showed kidney dysfunction as proteinuria excretion rate, podocalyxin excretion rates, renal monocyte chemoattractant protein-1 (MCP-1), blood urea nitrogen (BUN) and plasma creatinine were significantly increased as well as tubular degeneration occur. The significant decrease in renal reduced glutathione (GSH) level, superoxide dismutase (SOD) and catalase (CAT) activities and an increase in thiobarbituric acid reactive substances (TBARs) level, indicated that GEN-induced nephrotoxicity through oxidative stress reactions. Also, GEN up-regulated both gene expression and renal levels of inflammatory cytokines TNF-alpha and IL-6. On the other hand, concurrent treatment of gossypin plus GEN protected kidney tissues against nephrotoxic effects of GEN through elevated levels of renal GSH, SOD and CAT activities while decreased in renal TBARs level. In addition, gossypin down-regulated gene expression and renal levels of inflammatory cytokines TNF-alpha and IL-6 induced by GEN. SIGNIFICANCE: This study revealed that gossypin exerts protection against nephrotoxicity induced by gentamicin via its antioxidant activity. CI - Copyright (c) 2017 Elsevier Inc. All rights reserved. FAU - Katary, Mohamed AU - Katary M AD - Pharmacology and Toxicology Department, Faculty of Pharmacy, Damanhour University, Egypt. FAU - Salahuddin, Ahmad AU - Salahuddin A AD - Biochemistry Department, Faculty of Pharmacy, Damanhour University, Egypt. Electronic address: salahuddin@pharm.dmu.edu.eg. LA - eng PT - Journal Article DEP - 20170314 PL - Netherlands TA - Life Sci JT - Life sciences JID - 0375521 RN - 0 (Ccl2 protein, rat) RN - 0 (Chemokine CCL2) RN - 0 (Flavonoids) RN - 0 (Gentamicins) RN - 0 (Interleukin-6) RN - 0 (Sialoglycoproteins) RN - 0 (Thiobarbituric Acid Reactive Substances) RN - 0 (Tumor Necrosis Factor-alpha) RN - 0 (podocalyxin) RN - A3Q367XWX9 (gossypin) RN - EC 1.11.1.6 (Catalase) RN - EC 1.15.1.1 (Superoxide Dismutase) SB - IM MH - Animals MH - Catalase/metabolism MH - Chemokine CCL2/metabolism MH - Flavonoids/*pharmacology MH - Gentamicins/*adverse effects/pharmacology MH - Interleukin-6/metabolism MH - *Kidney/metabolism/pathology MH - Male MH - *Proteinuria/chemically induced/metabolism/pathology/prevention & control MH - Rats MH - Sialoglycoproteins/metabolism MH - Superoxide Dismutase/metabolism MH - Thiobarbituric Acid Reactive Substances/metabolism MH - Tumor Necrosis Factor-alpha/metabolism OTO - NOTNLM OT - Antioxidant OT - Gentamicin OT - Gossypin OT - IL-6 OT - Monocyte chemoattractant protein-1 OT - Nephrotoxicity OT - TNF-alpha EDAT- 2017/03/18 06:00 MHDA- 2017/04/30 06:00 CRDT- 2017/03/18 06:00 PHST- 2016/12/29 00:00 [received] PHST- 2017/03/08 00:00 [revised] PHST- 2017/03/12 00:00 [accepted] PHST- 2017/03/18 06:00 [pubmed] PHST- 2017/04/30 06:00 [medline] PHST- 2017/03/18 06:00 [entrez] AID - S0024-3205(17)30092-9 [pii] AID - 10.1016/j.lfs.2017.03.009 [doi] PST - ppublish SO - Life Sci. 2017 May 1;176:75-81. doi: 10.1016/j.lfs.2017.03.009. Epub 2017 Mar 14.