Figure 6.
Application of FGF7 improves both the hepatocyte damage and cholestatic liver injury. (A) Schematic representation of the experiment. Eight-week-old FGF7 Tg and control mice were subjected to the DDC-induced liver injury model or left untreated, and 1 wk later, Dox administration was started for FGF7 induction. After 3 wk of treatment, serum and liver samples were harvested for subsequent analyses. (B) Serum TBIL, ALP, AST, and ALT levels were measured in control and FGF7 Tg mice fed a normal (control, n = 3; Tg, n = 3) or DDC-containing (control, n = 9; Tg, n = 7) diet. Mean ± SE. (***) P < 0.001; (*) P < 0.05; (NS) not significant. (C) Typical skin color (right foot) of the DDC-treated animals at the end of the protocol, indicating that FGF7 Tg mice suffered less from jaundice than control mice. (D) Hematoxylin and eosin staining of livers from DDC-treated animals at the end of the protocol. Bars, 200 μm. (PV) Portal vein. (E) Immunostaining of CK19 (red) and A6 (green) in the livers of FGF7 Tg mice and control mice at the end of the protocol. Note that A6+ CK19− newly formed hepatocytes were increased in the livers of FGF7 Tg mice. Bars, 100 μm. (PV) Portal vein.
