Hepatic TGFβr1 deletion inhibited LPS/D-GalN–induced ALF. (A) Immunofluorescence co-staining of TGFβ1/F480 and TGFβ1/CD68 from WT mice with or without LPS/D-GalN co-injection (n = 5). (B) Immunohistochemistry staining of TGFβr1 in livers and (C) quantitative results (n = 5). (D) Schematic protocol used for reproducing TGFβr1Δhep-CKO mice. (E) Western blots of TGFβr1 in liver tissues and quantitative results of TGFβr1/GAPDH (n = 3). (F) Serum ALT and AST levels of TGFβr1Δhep-CKO and TGFβr1Δhep mice after vehicle or LPS/D-GalN treatment (n = 5). (G) H&E staining was performed on paraffin-embedded sections of mouse livers from TGFβr1Δhep-CKO and TGFβr1Δhep mice after vehicle or LPS/D-GalN treatment (n = 5). (H) Representative pictures for TUNEL assay and Ki67 immunofluorescence staining TGFβr1Δhep-CKO and TGFβr1Δhep mice after vehicle or LPS/D-GalN treatment (n = 5). (I) Western blot analyses of BCL2 and cl-caspase 8 proteins of TGFβr1Δhep-CKO and TGFβr1Δhep mice after vehicle or LPS/D-GalN treatment and their (J) ratios of each protein to GAPDH (n = 6). Scale bars: 100 μm; Data are presented as means ± SEM. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001. DAPI, 4′,6-diamidino-2-phenylindole; D-GalN, D-galactosamine; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.