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Caffeic acid phenethyl ester suppresses oxidative stress in Escherichia coli-induced pyelonephritis in rats.
- Source :
- Molecular & Cellular Biochemistry; Mar2007, Vol. 297 Issue 1/2, p131-138, 8p
- Publication Year :
- 2007
-
Abstract
- Abstract??Although oxidative damage is known to be involved in inflammatory-mediated tissue destruction, modulation of oxygen free radical production represents a new approach to the treatment of inflammatory diseases. Caffeic acid phenethyl ester (CAPE), an active component of propolis from honeybee hives, has antioxidant, anti-inflammatory and antibacterial properties. For that reason, we aimed to investigate the efficiency of CAPE administration in preventing oxidative damage in pyelonephritis (PYN) caused byEscherichia coli. In this study, 35 Wistar rats were grouped as follows: control, PYN 24?h, PYN 48?h, PYN 72?h, CAPE 24?h, CAPE 48?h and CAPE 72?h.E. coli(1???10<superscript>9</superscript>c.f.u.) were inoculated into the rats in both PYN and CAPE groups via urethral catheterization. Ten ?M/kg-body weight CAPE was injected to the rats in all CAPE groups 24?h beforeE. coliinfection, and injections were repeated at 24-h intervals. Rats were sacrificed 24?h, 48?h and 72?h after infection in both PYN and CAPE groups. Malondialdehyde (MDA) and nitric oxide (NO) levels were significantly increased in kidneys of PYN groups. The activities of the antioxidant enzymes, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and xanthine oxidase (XO) were also elevated byE. coli. However, CAPE administration reduced MDA and NO levels, as well as XO activity, although it increased SOD and GSH-Px activities. Histopathological examination showed that CAPE reduced the inflammation grade induced byE. coli. In conclusion, CAPE administrations decrease the oxidative damage occurring in PYN and therefore could be used for medical management of bacterial nephropathy. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 03008177
- Volume :
- 297
- Issue :
- 1/2
- Database :
- Complementary Index
- Journal :
- Molecular & Cellular Biochemistry
- Publication Type :
- Academic Journal
- Accession number :
- 24398055
- Full Text :
- https://doi.org/10.1007/s11010-006-9337-x