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.

Evaluation of the Mutagenic Properties of Two Lignans from Acanthopanax koreanum Nakai

Acanthopanax koreanum Nakai, a well known traditional herb grown in Jeju Island, South of Korea, has been used as a tonic and sedative agent, as well as in the treatment of diabetes and immune diseases. Mutagenicity of two lignans, syringaresinol and tortoside A isolated from A. koreanum, was assessed using Salmonella/microsome (Ames) test. Tester strains used were Salmonella typhimurium TA98, TA100, TA1535, and Escherichia coli WP2uvrA. The mutagenic activity was determined both in the absence or presence of S9 mixture. As a result, tortoside A did not cause any increase in the number of his+ revertants in S. typhimurium and E. coli WP2uvrA strains in the presence or absence of S9 mix, compared to the controls. Similarly, low concentrations of syringaresinol (750 and 1,500 microg/plate) did not show any mutagenic properties in all bacterial strains, in the presence or absence of S9 mixture. However, in the high concentration of syringaresinol (3,000 microg/plate), the number of revertants were increased in TA1535 strains, in the absence of S9 metabolic activation. Therefore, in vivo experiments such as comet assay are needed to further determine the genotoxic/carciogenic potential of syringaresinol isolated from A. koreanum.

The Effect of Diterpenoid Extracted from Acanthopanax Koreanum on the Collagen Indkuced Arthritis in DBA/1 Mice / 대한류마티스학회지

OBJECTIVE: No medication currently available for the treatment of rheumatoid arthritis is universally effective, and all can produce adverse effects. It is well known that the Acanthopanax koreanum extract has an anti-inflammatory action without any adverse effects reported. It is also reported that diterpenoid which is a partially purified product ectracted from Acanthopanax koreanum has an anti-inflammatory effect. We conducted this study whether diterpenoid extracted from Acanthopanax koreanum has a regressive effect of collagen induced arthritis in DBA/1 mice. METHODS: Four groups of DBA/1 mice were immunized by intradermal injection of 1mg/kg chicken type II collagen with complete Freund's adjuvant. Group II received 5mg/kg of diterpenoid extracted from Acanthopanax koreanum orally daily and Group III receive 5mg/kg of phenylpropranoids extracted from Acanthopanax koreanum orally daily. Group IV received 1mg/kg dexamathasone intraperitoneally twice weekly. Group I received no treatment. The prevalence of arthritis were assessed twice weekly. Seoum anti-collagen antibody was measured by ELISA. Stimulation index of caltured splenocytes were measured. Tumor necrosis factor-alpha and interleukin-10 levels in the supernatant of cultured splenocytes stimulated with Con. A were also measured by ELISA. RESULT: Collagen induced arthritis(CIA) started to develop 5 weeks after collagen injections. In diterpenoid treated group, CIA seemed to be regressed, but in phenylpropranoid group, regressive effect of artiritis was not observed. In dexamathasone treated group, both of suppression of CIA could be observed. Levels of anti-collagen antibodies were reduced in dexamethasone treated group, but not in both diterpenoid and phenylpropranoid group. No significant differences of splenic mononuclear cell SI among the groups was observed. There was an increased secretion of interleukin-10 in the supernatant of cultured splenocytes stimulated by Con A of the diterpenoid treated group. CONCLUSION: These findings showed that the diterpenoid extracted from Acanthopanax koreanum have an effect on supression of CIA.

The Effect of Acanthopanax Koreanum Extract on the Induction of Collagen Induced Arthritis for DBA / 1J Mice / 대한류마티스학회지

OBJECTIVE: No medication currently available for the treatment of rheumatoid arthritis is universally effective, and all can produce adverse effects. It is well known that the Acanthopanax koreanum extract has an anti-inflammatory action without any adverse effects reported. We conducted this study whether the Acanthopanax koreanum extract has a preventive and/or regressive effect of collagen induced arthritis in DBA/1J mice. METHODS: Three groups of BDA/1J mice were immunized by intradermal injection of 5ma/ka bovine type lI collagen with complete Freund s adjuvant. Group received 20ma/ka of Acanthopanax koreanum extract orally twice weekly and group K received 1ma/ka dexamethasone intraperitoneally twice weekly. Group ll and lll were divided into two subgroups respectively(Group Il-A, E-B, lll-A and Ill-B). Subgroup A is prevention group(Drugs were started to be given 3 weeks after immunization) and subgroup B is suppression group(Drugs were started to be given 6 weeks after immunization when CIA had been developed already). Group I received no treatment. The prevalence of arthritis were assessed twice weekly. Serum anti-collagen antibody and splenic mononuclear cell stimulation indices (SI) to collagen were measured. Serum tumor necrosis factor-a and interleukin-10 levels were also measured by ELISA. RESULT: Collagen induced arthritis(CIA) started to develop 4 weeks after collagen injections. In Acanthopanax koreanum extract treated group, CIA induction seemed not to be inhibited, but questionably partial supressive effect of arthritis were observed at 10 weeks after collagen injection. In dexamethasone treated group, both of prevention and suppression of CIA could be observed. Levels of anti-collagen antibodies were reduced in dexamethasone treated group, but not in the Acanthopanax koreanum extract treated group. No significant differences of splenic mononuclear cell SI among the groups was observed. There were no significant differences in the levels of serum tumor necrosis factor-a and interleukin-10 among the groups. CONCLUSIONS: These findings showed that the Acanthopanax koreanum extract does not have a definite effect on induction or supression of CIA.

The Effect of Acanthopanax koreanum Extract on the Induction of Collagen Induced Arthritis for DBA/1J Mice

PURPOSE: It is well known that the Acanthopanax koreanum extract has an anti-inflammatory action without any adverse effects reported. We conducted this study to see whether the Acanthopanax koreanum extract has a preventive effect on the development of collagen induced arthritis in DBA/1J mice. METHODS: Three groups of BDA/1J mice were immunized by intradermal injection of 2mg/kg bovine type II collagen with complete Freund' s adjuvant. Group I received 20mg/kg of Acanthopanax koreanum extract orally twice weekly and group II received 1mg/kg dexamethasone intraperitoneally twice weekly. Group III received no treatment. The prevalence of arthritis were assessed twice weekly. Serum anti-collagen antibody and splenic mononuclear cell stimulation indices (SI) to collagen were measured. Serum tumor necrosis factor-alpha levels were also measured by ELISA. RESULTS: Collagen induced arthritis (CIA) started to develop 5 weeks after collagen injections. In Acanthopanax koreanum extract treated group, CIA induction seemed to be inhibited as well as in dexamethasone treated group. However, they were not significant statistically. There was a significant increase in the serum levels of anticollagen antibody in the Acanthopanax koreanum extract treated group compared with rest of two groups, but no significant differences of splenic mononuclear cell SI among the groups. Serum tumor necrosis factor-alpha was decreased in the Acanthopanax koreanum extract treated group compared to the other two groups. CONCLUSION: These findings show that the Acanthopanax koreanum extract had no definite preventive effect on the development of CIA.