Fig. 2.

ROS mediates the expression of FGF10 in HSCs, while FGF10 acts through FGFR2b on hepatocytes. (A) Protein expression levels of α-SMA and FGF10 in primary HSCs treated with or without H₂O₂ (100 μM for 6 h). (B) Protein expression levels of α-SMA and FGF10 in primary HSCs treated with saline or NAC (1 mM added in the culture medium of the reoxygenation phase for 6 h) under control or H/R stimulation. (C) Protein expression levels of phosphorylated FRS2α, phosphorylated AKT, and total AKT in primary hepatocytes transfected with scramble siRNA or FGFR2 siRNA and then treated with saline or rFGF10 (1 μM for 1 h). (D) Protein expression levels of phosphorylated FRS2α, phosphorylated AKT, and total AKT in primary hepatocytes transfected with scramble siRNA or FGFR1 siRNA and then treated with saline or rFGF10 (1 μM for 1 h). For (A–D), GAPDH was served as the loading control; For (C–D), cells were serum starved for 12 h before rFGF10 treatment. All data are presented as mean ± SD, #P < 0.05. Con: control; N.S.: non-significant.