Lithium carbonate used in the long-term treatment of
manic-depressive illness has been reported to lead to progressive renal impairment in rats and humans.
Caffeic acid phenethyl ester (CAPE), a component of honeybee
propolis, protects tissues from reactive oxygene species mediated oxidative stress in
ischemia-reperfusion and toxic
injuries. The beneficial effect CAPE on
lithium-induced nephrotoxicity has not been reported yet. The purpose of this study was to examine a possible renoprotective effect of CAPE against
lithium-induced nephrotoxicity in a rat model. Twenty-two adult male rats were randomly divided into three experimental groups, as follows: control group,
lithium-treated group (Li), and
lithium plus CAPE-treated group (Li+CAPE). Li were treated intraperitoneally (i.p.) with 25 mg/kg Li2CO3
solution in
0.9% NaCl twice daily for 4 weeks. CAPE was co-administered i.p. with a dose of 10 microM/kg/day for 4 weeks. Serum Li, blood
urea nitrogen and plasma
creatinine, urinary
N-acetyl-beta-D-glucosaminidase (NAG, a marker of renal tubular injury), and
malondialdehyde (MDA, an index of lipid peroxidation), were used as markers of oxidative stress-induced renal impairment in Li-treated rats.
Superoxide dismutase (SOD),
catalase (CAT), and
glutathione peroxidase (GSH-Px) activities were studied to evaluate the changes of
antioxidant status in renal tissue. Serum Li levels were found high in the Li and Li+CAPE groups. In Li-administrated rats, urinary NAG and renal MDA levels were increased according to control and Li+CAPE groups (p < 0.05). CAPE caused a significant reduction in the levels of these parameters. Likewise, renal SOD, CAT and GSH-Px activities were decreased in Li-administrated animals; CAPE caused a significant increase in the activities of these
antioxidant enzymes. In conclusion, CAPE treatment has a protective effect against Li-induced renal tubular damage and oxidative stress in a rat model.