This study was carried out to investigate the protective effect of
troxerutin against
D-galactose (D-gal)-induced renal injury in mice.
Hematoxylin and
eosin (H&E) stained sections of kidneys revealed D-gal could cause renal injury and
troxerutin could significantly attenuate the injury. We further investigated the mechanisms involved in the protective effects of
troxerutin on mouse kidney. The following
antioxidant defense
enzymes were measured: cytosolic
Cu/Zn superoxide dismutase (SOD-1),
catalase (CAT) and
glutathione peroxidase (GPx). The content of the lipid peroxidation product
malondialdehyde (MDA) was also analyzed. In D-gal-treated mice,
antioxidant enzymes activities were significantly decreased and the level of MDA was significantly higher than those in the vehicle controls. Our results indicated that the protective effect of
troxerutin against D-gal induced renal injury might be caused, at least in part, by increasing the activity of
antioxidant enzymes with a reduction in lipid peroxidation product. Furthermore, we also examined the inflammatory signal mediators of
nuclear factor-kappaB (
NF-kappaB),
inducible nitric oxide synthase (iNOS),
cyclooxygenase-2 (COX-2) and
prostanoid receptor subtype EP2 by Western blot.
After treatment with D-gal, the
NF-kappaB p65, iNOS, COX-2 and EP2 were markedly upregulated. Upon co-treatment with the
troxerutin, however, the expressions of the
NF-kappaB p65, iNOS, COX-2 and EP2 markedly reduced, compared to D-gal treatment alone. These results indicated that
troxerutin has significantly inhibitory effects on the
NF-kappaB-mediated inflammatory response. These findings suggest
troxerutin could attenuate renal injury induced by D-gal probably through its
antioxidant and anti-
inflammation properties.