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Rosiglitazone, peroxisome proliferator receptor-gamma agonist, ameliorates gentamicin-induced nephrotoxicity in rats.
Int Urol Nephrol. 2010 Sep; 42(3):579-87.IU

Abstract

Nephrotoxicity is a major complication of gentamicin (GEN), which is widely used in the treatment of severe gram-negative infections. Reactive oxygen spaces (ROS) are important mediators of gentamicin-induced nephrotoxicity. Peroxisome proliferator-activated receptors (PPARs) have different activities including antioxidant properties. This study was performed to investigate the protective role of PPAR-γ agonist against GEN-induced nephrotoxicity. Male Wistar Albino rats were randomly divided into the following four groups, each of which consisted of six animals: (1) control; (2) intraperitoneally injected with GEN for 14 consecutive days (100 mg/kg/day); (3) treatment with rosiglitazone (RSG) via nasogastric gavage (10 mg/kg/daily for 14 days); (4) treatment with GEN + RSG combination for 14 day. Rats were decapitated on the 15th day and kidneys were removed. Urine was collected for every 24 h for the determination of daily urine volume. Urea, creatinine, Na(+) and K(+) levels were measured in blood. Malondialdehyde (MDA), reduced glutathione (GSH), and nitric oxide (NO) levels along with glutathione peroxidase (GSH-Px), catalase (CAT), and superoxide dismutase (SOD) activities were determined in the renal tissue. Changes in body weight were recorded. GEN treatment was found to cause nephrotoxicity as evidenced by elevation of serum urea and creatinine levels. Renal impairment was also assessed by the renal histology. The significant decrease in GSH and increases in MDA and NO levels as well as a decrease in GSH-Px, CAT, and SOD activities indicated that GEN-induced renal damage was mediated through oxidative reactions. On the other hand, RSG administration protected kidney tissue against GEN-induced and free radical-mediated oxidative renal damage in rats.

Authors+Show Affiliations

Department of Urology, Bezm-i Alem Valide Sultan Vakif Gureba Research and Education Hospital, Aksaray, Istanbul, Turkey.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

19779845

Citation

Ozbek, Emin, et al. "Rosiglitazone, Peroxisome Proliferator Receptor-gamma Agonist, Ameliorates Gentamicin-induced Nephrotoxicity in Rats." International Urology and Nephrology, vol. 42, no. 3, 2010, pp. 579-87.
Ozbek E, Ilbey YO, Simsek A, et al. Rosiglitazone, peroxisome proliferator receptor-gamma agonist, ameliorates gentamicin-induced nephrotoxicity in rats. Int Urol Nephrol. 2010;42(3):579-87.
Ozbek, E., Ilbey, Y. O., Simsek, A., Cekmen, M., Mete, F., & Somay, A. (2010). Rosiglitazone, peroxisome proliferator receptor-gamma agonist, ameliorates gentamicin-induced nephrotoxicity in rats. International Urology and Nephrology, 42(3), 579-87. https://doi.org/10.1007/s11255-009-9645-7
Ozbek E, et al. Rosiglitazone, Peroxisome Proliferator Receptor-gamma Agonist, Ameliorates Gentamicin-induced Nephrotoxicity in Rats. Int Urol Nephrol. 2010;42(3):579-87. PubMed PMID: 19779845.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Rosiglitazone, peroxisome proliferator receptor-gamma agonist, ameliorates gentamicin-induced nephrotoxicity in rats. AU - Ozbek,Emin, AU - Ilbey,Yusuf Ozlem, AU - Simsek,Abdulmuttalip, AU - Cekmen,Mustafa, AU - Mete,Fatih, AU - Somay,Adnan, Y1 - 2009/09/25/ PY - 2008/10/24/received PY - 2009/09/09/accepted PY - 2009/9/26/entrez PY - 2009/9/26/pubmed PY - 2011/3/1/medline SP - 579 EP - 87 JF - International urology and nephrology JO - Int Urol Nephrol VL - 42 IS - 3 N2 - Nephrotoxicity is a major complication of gentamicin (GEN), which is widely used in the treatment of severe gram-negative infections. Reactive oxygen spaces (ROS) are important mediators of gentamicin-induced nephrotoxicity. Peroxisome proliferator-activated receptors (PPARs) have different activities including antioxidant properties. This study was performed to investigate the protective role of PPAR-γ agonist against GEN-induced nephrotoxicity. Male Wistar Albino rats were randomly divided into the following four groups, each of which consisted of six animals: (1) control; (2) intraperitoneally injected with GEN for 14 consecutive days (100 mg/kg/day); (3) treatment with rosiglitazone (RSG) via nasogastric gavage (10 mg/kg/daily for 14 days); (4) treatment with GEN + RSG combination for 14 day. Rats were decapitated on the 15th day and kidneys were removed. Urine was collected for every 24 h for the determination of daily urine volume. Urea, creatinine, Na(+) and K(+) levels were measured in blood. Malondialdehyde (MDA), reduced glutathione (GSH), and nitric oxide (NO) levels along with glutathione peroxidase (GSH-Px), catalase (CAT), and superoxide dismutase (SOD) activities were determined in the renal tissue. Changes in body weight were recorded. GEN treatment was found to cause nephrotoxicity as evidenced by elevation of serum urea and creatinine levels. Renal impairment was also assessed by the renal histology. The significant decrease in GSH and increases in MDA and NO levels as well as a decrease in GSH-Px, CAT, and SOD activities indicated that GEN-induced renal damage was mediated through oxidative reactions. On the other hand, RSG administration protected kidney tissue against GEN-induced and free radical-mediated oxidative renal damage in rats. SN - 1573-2584 UR - https://www.unboundmedicine.com/medline/citation/19779845/Rosiglitazone_peroxisome_proliferator_receptor_gamma_agonist_ameliorates_gentamicin_induced_nephrotoxicity_in_rats_ DB - PRIME DP - Unbound Medicine ER -