Fig. 3. Hepatocyte-specific deletion of p38a ameliorates liver injury and oxidative stress in HFD+Cxcl1-treated mice.
WT and p38aHep−/− mice were fed an HFD for 3 months and injected with Ad-Cxcl1 for 2 weeks (n=8-9/group). (A) Body weight of mice was measured. (B) Body weight, liver weight, and liver triglyceride content at sacrifice. (C, D) Serum ALT levels before Ad-Cxcl1 infection and 2 weeks after Ad-Cxcl1 infection. The number of TUNEL+ hepatocytes/field at sacrifice were statistically compared (panel D, right). The representative images for TUNEL staining are included in Supporting Fig. S5B. (E-F) Liver tissues were subjected to western blot analyses of factors involved in apoptosis and ER stress (panel E), and the blots were quantified (panel F). p38α western blot images were obtained with an antibody specific to p38α isoform. Values represent mean ± SEM. Statistical evaluation was performed by Student’s t-test or one-way ANOVA with Tukey’s post hoc test for multiple comparisons (*p<0.05; **p<0.01). N.S., not significant; TG: triglyceride; Cl. CASP3, cleaved form of CASP3; MW, molecular weight.