Novel evidence suggesting an anti-oxidant property for erythropoietin on vancomycin-induced nephrotoxicity in a rat model

被引:75
作者
Cetin, Hasan [1 ]
Olgar, Seref
Oktem, Faruk
Ciris, Metin
Uz, Efkan
Aslan, Cagatay
Ozguner, Fehmi
机构
[1] Suleyman Demirel Univ, Fac Med, Dept Pediat, TR-32100 Isparta, Turkey
[2] Suleyman Demirel Univ, Fac Med, Dept Med Biol, Isparta, Turkey
[3] Suleyman Demirel Univ, Fac Med, Dept Internal Med, Isparta, Turkey
[4] Suleyman Demirel Univ, Fac Med, Dept Physiol, Isparta, Turkey
关键词
erythropoietin; nephrotoxicity; oxidative stress; vancomycin;
D O I
10.1111/j.1440-1681.2007.04695.x
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
1. The aim of the present study was to investigate the role of oxidative stress in renal injury and to determine whether erythropoietin (EPO) acts as an anti-oxidant in vancomycin (VCM)-induced renal impairment. 2. Twenty-four rats were divided into three groups as follows: (i) control (Group 1); (ii) VCM treated (Group 2); and (iii) VCM + EPO treated (Group 3). Vancomycin (200 mg/kg, i.p.) was administered to Groups 2 and 3 for 7 days. Erythropoietin (150 IU/kg, i.p.) treatment was started 24 h before VCM and lasted for 7 days. On Day 8, renal tissues were excised and blood samples were collected. Serum creatinine and blood urea nitrogen were measured, along with renal malondialdehyde (MDA) levels, superoxide dismutase (SOD) and catalase (CAT) activity and tissue VCM levels. The kidneys were examined for any histopathological changes. 3. Renal MDA levels were found to be increased, whereas SOD and CAT activity was decreased, in the VCM-treated group compared with the control group. There was a marked decrease in MDA levels and an increase in SOD activity, but not CAT activity, after VCM + EPO treatment. Marked histopathological alterations, including interstitial oedema, tubular dilatation, tubular epithelial cell desquamation and vacuolization, were observed in VCM-treated rats. Histopathological changes were significantly improved after EPO administration. 4. In conclusion, the present data suggest that oxidative stress plays an important role in VCM-induced nephrotoxicity. Erythropoietin seems to act as an anti-oxidant, diminishing the toxic oxidative effects of VCM on renal tissues.
引用
收藏
页码:1181 / 1185
页数:5
相关论文
共 35 条
[1]  
AEBI H, 1984, METHOD ENZYMOL, V105, P121
[2]   VANCOMYCIN AND THE KIDNEY [J].
APPEL, GB ;
GIVEN, DB ;
LEVINE, LR ;
COOPER, GL .
AMERICAN JOURNAL OF KIDNEY DISEASES, 1986, 8 (02) :75-80
[3]   Protective effect of erythropoietin on renal ischemia and reperfusion injury [J].
Ates, E ;
Yalcin, AU ;
Yilmaz, S ;
Koken, T ;
Tokyol, C .
ANZ JOURNAL OF SURGERY, 2005, 75 (12) :1100-1105
[4]   Erythropoietin enhances recovery after cisplatin-induced acute renal failure in the rat [J].
Bagnis, C ;
Beaufils, H ;
Jacquiaud, C ;
Adabra, Y ;
Jouanneau, C ;
Le Nahour, G ;
Jaudon, MC ;
Bourbouze, R ;
Jacobs, C ;
Deray, G .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 2001, 16 (05) :932-938
[5]   In vitro and in vivo evidence suggesting a role for iron in cisplatin-induced nephrotoxicity [J].
Baliga, R ;
Zhang, ZW ;
Baliga, M ;
Ueda, N ;
Shah, SV .
KIDNEY INTERNATIONAL, 1998, 53 (02) :394-401
[6]   EFFECTS OF DAPTOMYCIN AND VANCOMYCIN ON TOBRAMYCIN NEPHROTOXICITY IN RATS [J].
BEAUCHAMP, D ;
PELLERIN, M ;
GOURDE, P ;
PETTIGREW, M ;
BERGERON, MG .
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, 1990, 34 (01) :139-147
[7]   Erythropoietin protects against brain ischemic injury by inhibition of nitric oxide formation [J].
Calapai, G ;
Marciano, MC ;
Corica, F ;
Allegra, A ;
Parisi, A ;
Frisina, N ;
Caputi, AP ;
Buemi, M .
EUROPEAN JOURNAL OF PHARMACOLOGY, 2000, 401 (03) :349-356
[8]   RECOMBINANT-HUMAN-ERYTHROPOIETIN STIMULATES ANGIOGENESIS IN-VITRO [J].
CARLINI, RG ;
REYES, AA ;
ROTHSTEIN, M .
KIDNEY INTERNATIONAL, 1995, 47 (03) :740-745
[9]   Protective effects of different antioxidants and amrinone on vancomycin-induced nephrotoxicity [J].
Celik, I ;
Cihangiroglu, M ;
Ilhan, N ;
Akpolat, N ;
Akbulut, HH .
BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY, 2005, 97 (05) :325-332
[10]  
DRAPER HH, 1990, METHOD ENZYMOL, V186, P421