Effect of mangiferin on mRNA expression of transforming growth factor beta in rats with liver fibrosis induced by thioacetamide

The bioactive compound mangiferin is known for its inhibition of fibrosis, a process that is reversible as a result of a liver injury. In this study, we aimed to explore the possible antifibrotic effect of mangiferin through the inhibition of mRNA expression of transforming growth factor beta (TGF-β), which is the primary profibrogenic cytokine. We induced liver fibrosis in rats by intraperitoneally injecting them with thioacetamide 200 mg/kg three times per week for 5 weeks. We gave mangiferin orally at a dose of 50 mg/kg/day and 100 mg/kg/day for 5 weeks. We had the following four treatment groups: the control group, the thioacetamide only group, the thioacetamide + mangiferin 50 mg/kg/day group, and the thioacetamide + mangiferin 100 mg/kg/day group. We measured the expression of TGF-β mRNA with qRT-PCR and calculated it using the Livak method. We found an increased expression of TGF-β mRNA in the group that was administered only thioacetamide compared it with that of the control group. In the treatment groups, we found a lower TGF-β mRNA expression than that in the thioacetamide-only group, but the only treatment achieving a statistically significant result compared with that of the thioacetamide only group was the group with mangiferin at a dose of 50 mg/kg BW. Mangiferin may, therefore, have a beneficial effect in inhibiting thioacetamide-induced fibrogenesis by lowering the mRNA expression of TGF-β.