Fig. 1

Ablation of Fkbp51 gene reduces CCl₄-induced liver damage. A Gross liver structure was observed in control and CCl₄-treated Fkbp51 KO and WT littermate mice. In WT liver with CCl₄ treatment, the fibrosis nodules are indicated by black arrows. B, C Serum analyses of Control and CCl₄-treated Fkbp51 KO and WT were performed to determine the concentrations of AST and ALT. D Histological examination of Control and CCl₄-treated Fkbp51 KO and WT liver sections stained with Masson’s trichrome. Mice treated with CCl₄ displayed portal vein fibrosis and ballooning (star), and hepatocytes undergoing necrosis (arrow). E CCl₄-treated WT liver sections possess significantly higher hepatic fibrosis scores as compared to Fkbp51 KO liver. F Expression patterns of TIMP1 detected by IHC are higher in the liver sections of CCl₄-treated WT mice relative to KO mice. G Quantitation of AOD of TIMP1 in liver sections. H. Immunoblot and quantification showed less α-SMA protein in CCl₄-treated KO than WT. I TUNEL was performed to measure apoptosis in the liver. More apoptotic cells (indicated by arrows) were found following CCl₄ treatment in WT than KO liver. J Quantitation of percentage TUNEL-positive hepatocytes (%) in liver sections. Graphs represent mean values ± SEM from 10 mice for each group. p values were determined by two-way ANOVA with the statistical significance labeled as follows: ** as p < 0.01, *** as p < 0.001 and **** as p < 0.0001. Key: WT, wild type; KO, Fkbp51 KO; AOD, average optical density