RESUMEN
Objective To study protective effects of acanthoic acid ( AA) against acute liver injury. Methods Sixty mice were randomly divided into six groups (n=10 each),including normal control group,model control group,positive control group (N-acetyl -L- cysteine,NAC,300 mg·kg-1),and AA at small (50 mg·kg-1),middle (100 mg·kg-1),and high (200 mg·kg-1 ) dose groups. Each group received respective treatment for 3 days and fasted for 16 h before the last dose. All animals except of the normal control group were treated with tacrine (35 mg·kg-1 ) 1 h after the treatments. Hepatic pathological and serum biochemical changes were observed. Results The high-dose of AA significantly reduced the levels of AST (143±46) U·L-1 ,ALT (32±9) U·L-1 ,LDH (1 218±312) U·L-1 ,MDA (3. 24±0. 48) μmol·g-1 ,and GSH (417±15) mg·g-1 compared with the model control group (P<0. 05 or P<0. 01). Liver injury was also ameliorated in AA high dose group.Conclusion AA has a protective effect on acute liver injury in mice.
RESUMEN
The hepatoprotective activity of Acanthopanax koreanum Nakai extract (AE) was investigated against D-Galactosamine/Lipopolysaccharide (D-GalN/LPS)-induced liver failure rats compared with that of acanthoic acid (AA) isolated from AE. Although D-GalN/LPS (250 mg/kg body weight/10 microg/kg body weight, i.p.) induced hepatic damage, pretreatments with AE (1 and 3% AE/g day) and AA (0.037% AA, equivalent to 3% AE/g day) alleviated the hepatic damage. This effect was the result of a significant decrease in the activity of alanine transaminase. Concomitantly, both the nitric oxide and IL-6 levels in the plasma were significantly decreased by high-dose AE (AE3) treatment compared to the GalN/LPS control (AE0). This response resulted from the regulation of pro-inflammatory signaling via a decrease in TLR4 and CD14 mRNA levels in the liver. While a high degree of necrosis and hemorrhage were observed in the AE0, pretreatment with AE3 and AA reduced the extent of hepatocyte degeneration, necrosis, hemorrhage and inflammatory cell infiltrates compared to the AE0. In conclusion, these results suggest that especially high-dose AE are capable of alleviating D-GalN/LPS-induced hepatic injury by decreasing hepatic toxicity, thereby mitigating the TLR 4-dependent cytokine release. The anti-inflammatory effect of AE could be contributing to that of AA and AE is better than AA.