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

Abstract

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.