We have shown that the orally administered
cyanidin 3-O-beta-D-glucoside (C3G) attenuates the hepatic
ischemia-reperfusion (I/R) injury, which was used as a model for oxidative stress through a decrease in neutrophil
chemoattractant production in rats. The rats were subjected to hepatic I/R at 30 min after the administration of C3G (0.9 mmol/kg
body weight) or vehicle. I/R treatment resulted in the elevation of oxidative stress marker [liver
thiobarbituric acid-reactive substance, Nepsilon-(hexanonyl)
lysine and
dityrosine] levels in the liver and of the serum activities of marker
enzymes for liver injury. The administration of C3G significantly suppressed these elevations, which had been caused by hepatic I/R. Liver
myeloperoxidase activity, a useful marker for neutrophil infiltration into tissues, and the plasma and liver concentration of
cytokine-induced neutrophil chemoattractant-1 (CINC-1), which has a potent chemotactic activity, were markedly elevated in the control group after hepatic I/R. However, these elevations were significantly suppressed in the C3G group. C3G and its metabolites in the plasma and liver were detected in the C3G group after hepatic I/R. These results suggest that the absorbed C3G and/or its metabolites can act as
antioxidants in the blood and liver and scavenge the
reactive oxygen species, and brought on a decrease in neutrophil infiltration into the liver through the suppression of CINC-1 production and the tissue damage caused by neutrophils after I/R is attenuated.