Protective effects of Acanthopanax koreanum Kakai extract against carbon tetrachloride-induced liver injury in Sprague-Dawley rats / 한국영양학회지

PURPOSE: This study was conducted in order to investigate the protective effects of ethanolic extract of Acanthopanax koreanum Nakai (AE) against carbon tetrachloride (CCl4)-induced liver injury in rats. METHODS: Male Sprague-Dawley rats were randomly divided into four groups in order to receive the following experimental diets with intraperitoneal injection of CCl4 (2.0 mL/kg body weight, 20% solution 0.65 mL) for eight weeks (n = 8 per group): CCl4 control (CON), CCl4 + AE 1% (AE1), CCl4 + AE 3% (AE3), or CCl4 + acanthoic acid 0.037%, which is equivalent to AE 3% (AA). RESULTS: Highest serum ALT activity and albumin level were observed in the CCL4 control group, but showed a significant decrease by either AE or AA supplementation in a dose-dependent manner (p = 0.0063 and 0.0076, respectively). Both hemotoxylin and eosin staining and Masson's staining indicated remarkable prevention of CCl4-induced liver damage in the AE3 group. TNFalpha and IL-6 production were significantly lowered in the AE treated groups, but not in the AA group (p = 0.0016 and p = 0.0002, respectively). The effects of AE3 were greater than those of AA for inflammation and liver toxicity biomarkers. CONCLUSION: Taken together, the results suggested that ethanolic extract of Acanthopanax koreanum Nakai provided hepa-toprotective effects, leading to the reduction of inflammatory response. In addition, the effect of AE was superior to that of single compound AA.

Acanthopanax koreanum Nakai modulates the immune response by inhibiting TLR 4-dependent cytokine production in rat model of endotoxic shock

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.