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Six groups of male Wistar rats were treated as follows: in groups II, III and V liver damage was induced by CCl(4) (per os, 1590 mg/kg b.w.day) given 2 days a week for 6 weeks; group III was treated simultaneously with ethanol extract of Aquilegia vulgaris (100 mg/kg b.w.day) for 6 weeks; group V with silymarin, positive control, at a dose of 100 mg/kg b.w.day for 6 weeks; and groups IV and VI received only the extract or silymarin, respectively. Microsomal lipid peroxidation in the liver increased following CCl(4) treatment by 61-213% and was not changed significantly by the extract. The effect of silymarin was more pronounced, 19-52% decrease in the lipid peroxidation level. Hepatic glutathione was depleted by 22% in CCl(4)-treated rats. The extract tested did not change this parameter. The activity of antioxidant enzymes was significantly reduced after CCl(4) administration, by 42-63%. Co-administration of the extract or silymarin resulted in significant increase in these enzymes activity; however, the basal level was not reached. Hepatic hydroxyproline concentration was elevated over 5-fold in comparison with controls. Co-administration of the extract or silymarin decreased the level of hydroxyproline by 66% and 55%, respectively. Activity of serum hepatic enzymes was elevated in rats treated with CCl(4) by 47-8700%. Both the extract and silymarin reduced significantly these enzymes' activity. The extract caused a fall in bilirubin and cholesterol level in rats treated with CCl(4) by 42% and 17%, respectively. Histopathological examination revealed less-severe fibrosis in rats co-administered the extract or silymarin when compared to animals treated with CCl(4) alone.

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.

The ethyl ether extract of A. vulgaris inhibited in vitro microsomal lipid peroxidation (IC50 58.8 microg/ml) and showed moderate ability to scavenge superoxide radicals and to chelate iron ions. The extract (100 mg/kg body weight, po) decreased uninduced and enzymatic microsomal lipid peroxidation in the liver of male rats pretreated with CCl4 (1 ml/kg body weight) by 27 and 40%, respectively. Activity of antioxidant and related enzymes (catalase and glucose-6-phosphate dehydrogenase) inhibited by CCl4 was significantly restored after administration of the extract. The extract itself significantly enhanced superoxide dismutase activity. There was no effect of the extract on hepatic glutathione level and cytochrome P450 content, both were decreased by CCl4. Neither CCl4 nor the tested extract affected activities of NADPH-cytochrome P450 reductase and two monooxygenases, aniline hydroxylase and aminopyrine n-demethylase. It can be concluded that the protective effect of the A. vulgaris extract in CCl4-induced liver injury is mediated by inhibition of microsomal lipid peroxidation and restoring activity of some antioxidant and related enzymes.

The hepatoprotective effect of the ethanol extract (AvEE) and the main fl avonoid compound 4'-methoxy-5,7-dihydroxy fl avone 6-C-beta-glucopyranoside (isocytisoside, ISOC) from the leaves and stems of Aquilegia vulgaris L. were studied using the CCl(4)-induced hepatotoxicity test. The acute toxicity test in mice showed that AvEE can be classi fi ed as nontoxic since a dose of 3000 mg/ kg did not cause mortality. The barbiturate-induced sleeping time prolonged by CCl(4) administration to mice was signi fi cantly reduced after AvEE treatment proving the protective effect of the extract on microsomal drug-metabolizing enzymes.AvEE and ISOC administered to rats 48 h, 24 h and 2 h before, and 6 h after CCl(4) intoxication caused a signi fi cant decrease in the CCl(4)-induced elevation of hepatic enzymes activity in serum, i.e. sorbitol dehydrogenase (SDH), glutamate oxaloacetate and glutamate pyruvate transaminases (GOT, GPT). Both substances induced CCl(4)-diminished erythrocyte superoxide dismutase (SOD) and reduced the activities of glutathione peroxidase (GPx) and glutathione reductase (GR) preliminarily enhanced by CCl(4). The hepatoprotective properties of AvEE and ISOC were con fi rmed by pathomorphological examination of the liver., (Copyright 2003 John Wiley & Sons, Ltd.)