Objective: To determine the effects of alpha-mangostin on thioacetamide (TAA)-induced liver cirrhosis in rats.
Material and Method: Male Wistar rats were divided into 3 groups and treated with intraperitoneal injections of TAA (200
mg/kg) 3 times per week for per week for 8, 12 and 16 weeks, respectively. One subgroup was left untreated whereas the other
two were treated either with 100 mg/kg α-mangostin or vehicle alone (80% DMSO, 20% water), which were administered
intraperitoneally 3 times per week for a total of 4 weeks. The incidence of fibrotic nodules on the liver and the serum levels of
the liver enzymes aspartate transaminase (AST) and alanine transaminase (ALT) were measured. Moreover, the liver cirrhosis-related genes expression and p53 protein level in liver were analyzed by quantitative reverse transcription PCR and
Western blot analysis, respectively.
Results: Fibrotic nodules on the liver were formed upon treatment with TAA for 12 or 16 weeks. The nodules were then
reduced by treatment with α-mangostin as compared to treatment with the vehicle DMSO. Moreover, the serum levels of the liver enzymes AST and ALT after treatment with α-mangostin decreased as compared to DMSO alone. The liver cirrhosisrelated genes expression showed no significant differences, whereas the p53 protein level in liver showed that α-mangostin reduced risk of liver fibrosis through the decrease in p53 expression as compared to the TAA_DMSO treatment.
Conclusion: The results suggest that α-mangostin has a beneficial therapeutic effect in the TAA liver cirrhosis model. Further investigations on mechanisms of α-mangostin as therapeutic agent should be determined.

Keywords: Cirrhosis, α-mangostin, Thioacetamide, Dimethyl sulfoxide