It was reported that
ipriflavone was primarily metabolized via hepatic
CYP1A1/2 and 2C11 in rats. In the present study, the expression of
CYP1A2 and 2C11 decreased in the liver, but increased in the intestine in rats pretreated with E. coli
lipopolysaccharide (ECLPS; an animal model of
inflammation). Thus, pharmacokinetic parameters of
ipriflavone and its metabolites, M1 and M5, were evaluated in ECLPS rats. After
intravenous administration (20 mg/kg) to ECLPS rats, the AUC of
ipriflavone was significantly greater (26.7% increase) and CL(NR) of
ipriflavone was significantly slower (19.9% decrease) than in the controls. This could have been due to decreased expression of hepatic
CYP1A2 and 2C11 compared to the controls. After
oral administration (200 mg/kg) to ECLPS rats, the AUC of
ipriflavone was also significantly greater (130% increase) than in the controls. Although the expression of intestinal
CYP1A2 and 2C11 increased in ECLPS rats, contribution of this increase to the significantly greater AUC of
ipriflavone after
oral administration of
ipriflavone to ECLPS rats was not considerable. This could have also been due to a significantly decreased expression of hepatic
CYP1A2 and 2C11 in ECLPS rats. The formation of M1 and M5 could be mediated via
CYP1A2 and/or 2C11 in rats.