OBJECTIVE: To investigate the hepatoprotective potential of n-butanolic extract of Astragalus monspessulanus L. (EAM) against in-vitro/in-vivo carbon tetrachloride (CCl4)-induced liver damage in rats. Silymarin was used as a positive control. METHODS AND RESULTS: The in-vitro experiments were carried out in primary isolated rat hepatocytes first incubated with CCl4 (86 µmol/l). Hepatic injury was discerned by a decrease in cell viability and cell glutathione (GSH) levels, an increase in lactate dehydrogenase leakage into the medium, and an elevation in malondialdehyde (MDA) quantity. Cell pre-incubation with EAM (1 µg/ml and 10 µg/ml) significantly ameliorated the CCl4-induced liver damage. In-vivo rats were challenged orally with CCl4 (10% solution in olive oil) alone and after 7 days pre-treatment with EAM (100 mg/kg body weight per day, oral gavage). CCl4 damage was judged by an increased production of MDA, depletion of cell GSH, and a decrease in cell antioxidant defense system. EAM pre-treatment normalizes the activities of the antioxidant enzymes and the levels of GSH and MDA. These data are supported by the histopathological examination. CONCLUSION: These results indicate that EAM has a similar significant protective effect, in vitro and in vivo, against CCl4 induced hepatotoxicity in rat as silymarin.This may be due to its antioxidant and membrane stabilizing properties.
OBJECTIVE: To investigate the hepatoprotective potential of n-butanolic extract of Astragalus monspessulanus L. (EAM) against in-vitro/in-vivo carbon tetrachloride (CCl4)-induced liver damage in rats. Silymarin was used as a positive control. METHODS AND RESULTS: The in-vitro experiments were carried out in primary isolated rat hepatocytes first incubated with CCl4 (86 µmol/l). Hepatic injury was discerned by a decrease in cell viability and cell glutathione (GSH) levels, an increase in lactate dehydrogenase leakage into the medium, and an elevation in malondialdehyde (MDA) quantity. Cell pre-incubation with EAM (1 µg/ml and 10 µg/ml) significantly ameliorated the CCl4-induced liver damage. In-vivo rats were challenged orally with CCl4 (10% solution in olive oil) alone and after 7 days pre-treatment with EAM (100 mg/kg body weight per day, oral gavage). CCl4 damage was judged by an increased production of MDA, depletion of cell GSH, and a decrease in cell antioxidant defense system. EAM pre-treatment normalizes the activities of the antioxidant enzymes and the levels of GSH and MDA. These data are supported by the histopathological examination. CONCLUSION: These results indicate that EAM has a similar significant protective effect, in vitro and in vivo, against CCl4 induced hepatotoxicity in rat as silymarin.This may be due to its antioxidant and membrane stabilizing properties.
Authors: R L Simeonova; V B Vitcheva; M S Kondeva-Burdina; I N Krasteva; S D Nikolov; M K Mitcheva Journal: Phytomedicine Date: 2010-02-02 Impact factor: 5.340