Introduction and Objectives
The purpose of the present study was to investigate the effects of caffeic acid phenethyl ester (CAPE) on cyclosporine A (CsA)-induced nephrotoxicity.
Material and Methods
Wistar-albino female rats, 250–300 g, were used in experiments. The animals were divided into four groups (n = 7). In control group rats were given 0.5 ml of normal saline s.c. daily for a period of 10 days. In CAPE group rats were treated with CAPE (10 μmol/kg/day) in 0.5 ml of normal saline i.p. daily for a period of 11 days. Rats in CsA group were injected with CsA s.c. in 0.5 ml of normal saline (15 mg/kg) once a day for 10 days. Finally in CsA+CAPE group rats were treated with CAPE (10 μmol/kg/day) in 0.5 ml of normal saline i.p. daily for a period of 11 days and rats were s.c. injected with CsA in 0.5 ml of normal saline (15 mg/kg) once a day for 10 days beginning from the second day of CAPE administration. After the last administration of the drug, all rats fasted about 12 hours, but had free access to water. At the end of the experiment blood was collected, serum were separated and used for various biochemical estimations. The renal tissue was excised immediately from the rats, washed with pre-chilled physical saline and used for further biochemical estimations. ANOVA test was performed and post hoc multiple comparisons were made using least-squares differences.
The administration of CsA alone resulted in higher myeloperoxidase (MPO) activity, lipid peroxidation, superoxide dismutase (SOD) and catalase (CAT) than in the control. The enzyme activities except CAT in rats treated with CAPE alone were not changed. CAPE treatment prevented the increase in malondialdeyde (MDA) and increased CAT activity more, but did not affect the activities of MPO and SOD enzymes (Table 1).
Table 1.The levels of BUN, Creatine, MDA and the activities of MPO, SOD and CAT enzymes in serum in control, CAPE, CsA and CsA+CAPE groups
|MDA (nmol/g protein)||MPO (U/g protein)||SOD (U/mg protein)||CAT (k/mg protein)||BUN (mg/dL)||Creatine (mg/dL)|
|Control (n = 7)||8.61±0.61||0.091±0.009||0.284±0.034||0.278±0.028||15.42±1.42||0.40±0.03|
|CAPE (n = 7)||10.11±0.68||0.112±0.008||0.353±0.037||0.335±0.005||15.14±0.55||0.41±0.04|
|CsA (n = 7)||11.32±0.75||0.126±0.005||0.544±0.061||0.361±0.017||22.28±1.44||0.52±0.03|
|CsA+CAPE (n = 7)||8.74±0.49|
Results are presented as mean±SEM
a p < 0.01 compared with control group.
b p < 0.001 compared with control group.
c p < 0.05 compared with CsA group.
d p < 0.01 compared with CsA group.
e p < 0.05 compared with control group.
We demonstrated an increase in lipid peroxidation and MPO, SOD and CAT activity in renal tissue of rats given CsA. Additionally lipid peroxidation-mediated renal injury was prevented partly by CAPE treatment. Our results collectively suggest that CAPE may be an available agent to protect the kidney from CsA induced damage via inhibition oflipid peroxidation.
© 2009 European Association of Urology. Published by Elsevier Inc. All rights reserved.