The phytochemical was able to maintain its hepatic function and architecture during fibrosis development in a CCl4-induced liver fibrosis mouse model by the direct inhibition of fibrosis-mediating proteins (e.g., the platelet-derived growth factor receptor beta, TIMP metallopeptidase inhibitor 1, Toll-like receptor 9 and TGF-β [9]. This evidence concerns the gene TGFB1 and Hepatic fibrosis.