Effect of Aquilegia vulgaris (L.) ethyl ether extract on liver antioxidant defense system in rats.

INTRODUCTION The ethyl ether extract from Aquilegia vulgaris (L.) (Ranunculaceae) contains a lot of phenolic acids. Their hydroxyl groups are capable of donating hydrogen atoms at the initial stage of lipid peroxidation (LPO), which inactivates hydroxyperoxides formed from polyunsaturated fatty acids (PUFAs) and leads to breakdown of the propagation chain. MATERIAL AND METHODS Rats pretreated with acetaminophen (APAP) (600 mg/kg b.w., p.o.) were given ethyl ether extract (100 mg/kg b.w., p.o.) obtained from A. vulgaris herb. The study parameters measured were microsomal lipid peroxidation, reduced glutathione, and the activity of hepatic antioxidant enzymes and some drug metabolizing enzymes. RESULTS The treatment with ethyl ether extract of the herb produced a 87-95% decrease in uninduced and Fe2+/ascorbate-stimulated microsomal lipid peroxidation in the liver of rats receiving APAP. Hepatic glutathione level depleted by APAP increased significantly (by 18%) after the extract treatment. Antioxidant enzyme activity in the liver, inhibited by APAP, was found to increase after administration of the extract: catalase by about 36%, glutathione reductase by 27% and glutathione S-transferase by 29%. Glucose-6-phosphate dehydrogenase, which decreased after APAP administration, increased again by 26% after extract treatment. The extract tested did not affect the activity of DT-diaphorase. The cytochrome P450 content, depleted by APAP, increased as much as by 100% after the treatment. The activities of NADPH-cytochrome P450 reductase, aniline hydroxylase and aminopyrine N-demethylase were not affected. CONCLUSIONS The protective effect of the Aquilegia vulgaris extract in APAP-induced liver injury was mediated by its antioxidant activity. The extract did not inhibit the formation of reactive intermediate metabolites of APAP.