In our ex vivo mouse liver fibrosis model induced by TGF-β1 (5 ng/mL), HE exhibited antifibrotic effects by reducing the expression of key fibrogenic genes (α-SMA, COL1A1, SERPINH-1, VIM and FN-1) and by inhibiting the TGF-β/SMAD2 signaling pathway, indicating a negative modulation of the central molecular axis driving early-stage hepatic fibrosis progression. Here, SMAD2 is linked to hereditary elliptocytosis.