Figure 7.
Forced expression of FXR ameliorates CCl4-induced hepatotoxicity in Fxr−/− mice. Adenovirus carrying mouse Fxr cDNA (Ad-Fxr) or empty vector (Ad-Ctrl) was injected to Fxr−/− mice and wild-type (WT) mice (2.0×109 pfu/mouse) 5 days before CCl4 injection (0.25 ml/kg). A, Serum AST, ALT, and TCA levels. B, Hepatic mRNA levels of genes encoding FXR-related proteins and genes encoding proinflammatory modulators. C, Western blot analysis of JNK. Whole liver lysates (20 μg of proteins) were electrophoresed and transferred to PVDF membrane for determining hepatic levels of total (T-) and phosphorylated (P-) JNK. The band of GAPDH was used as a loading control. D, Quantification of P-JNK. The band intensities of P-JNK and GAPDH were quantified using ImageJ software, and the ratio of P-JNK to GAPDH was calculated. Data are presented as the means ± SD and one-way ANOVA followed by Tukey’s post hoc correction was applied for comparisons. *P < .05; ***P < .001 versus all other groups.