Antifibrotic effects of 3,5-dicaffeoylquinic acid on in vivo model of liver fibrosis

초록

Aims of the study: Oxidative stress in the liver injury is a major pathogenetic factor in progress of liver fibrosis. Until now, it has not been reported that effective treatment of liver fibrosis is available for clinical use. In this study, we evaluated the protective effects of 3,5-dicaffeoylquinic acid, which is one of the major extract compound of Ilex rotunda Thunb, on dimethylnitrosamine (DMN)-induced liver fibrosis animal model. Materials and methods: DMN at a dose of 10 mg/kg were intraperitoneally injected into SD rats by 3 times per week for a month. At the same time, 100 mg/kg of 3,5-Dicaffeoylquinic acid was orally administrated. In other group as a control, water or 3,5-dicaffeoylquinic acid was orally administered. After the treatments, liver was recovered and biologically and histologically assessed. Biochemical markers (i.e., ALP, T-Bilirubin, and D-Bilirubin) and mRNA of fibrosis-related proteins were also evaluated. Results: Histology results showed that 3,5-dicaffeoylquinic acid suppressed the infiltration of inflammatory cells and fibrosis of liver tissue. In the DMN treating group, ALP, T-Bilirubin, and D-Bilirubin were highly increased compared to control (water treating group). On the other hand, the group of co-administration of 3,5-dicaffeoylquinic acid and DMN showed the significant lowered ALP, T-Bilirubin and D-Bilirubin levels. Body weight and liver weight in 3,5-dicaffeoylquinic acid-treated group were maintained in normal ranges compared. mRNA levels of collagen type 1 and alpha-SMA were not significantly increased in comparison with DMN group. Conclusion: Our results indicated that 3,5-dicaffeoylquinic acid has the potential of hepatoprotective and anti-fibrogenic effects against DMN-induced liver injury.