FIGURE 3.

Acute CCl₄-induced liver injury is ameliorated by the deficiency of IRF3 or inhibition of TBK1, independent of TRIM or TRAM, type I IFN signaling. A and B, WT or IRF3-KO mice received a single injection of CCl₄. Serum ALT levels were assessed (A), and apoptosis was assessed by measuring caspase-3 cleavage in the liver by immunoblot (B). C and D, WT or IFNAR1-KO mice received a single injection of CCl₄. Serum ALT levels were assessed (C), and IRF3 activation and apoptosis were assessed by probing for phosphor-IRF3 and caspase-3 cleavage in the liver by immunoblot (D). E and F, WT were pretreated with DMSO or BX795, a TBK1 inhibitor, 2 h before receiving a single injection of corn oil (vehicle) or CCl₄. Serum ALT levels were assessed (E), and IRF3 activation and apoptosis were assessed by probing for phosphor-IRF3 and caspase-3 cleavage in the liver by immunoblot (F). G and H, WT or TRIF- or TRAM-KO mice received a single injection of CCl₄. G and H, serum ALT levels were assessed (G), and IRF3 activation and apoptosis were assessed by probing for phosphor-IRF3 and caspase-3 cleavage in the liver by immunoblot (H). The mice were bled serially at the indicated time points. n = 8–9 mice (CCl₄-treated, per genotype); 3–4 mice (oil-treated, per genotype) (A, C, and G). n = 3–5 mice (CCl₄-treated, pretreated with BX795); 3 mice (oil-treated, pretreated with DMSO) (E).