Fig. 6

THBS1 deficiency alleviates D-gal/LPS-induced liver failure via anti-inflammatory enhancement and suppression of apoptosis. A Changes in hepatic expression of different inflammatory target genes following D-gal/LPS treatment in both WT and THBS1^KO mice. Data are represented as the mean ± SD, n = 10 for each time point. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 vs. WT; Gapdh was used as a reference control gene. B Representative western immunoblotting of THBS1 and major key targets of the apoptotic cascade in liver tissues collected from WT and THBS1^KO mice; β-actin was used as an internal control. C D-gal/LPS coadministration caused massive hepatocyte apoptosis (black arrow), characterized by the obvious positive TUNEL staining in the WT mice, whereas THBS1^KO prevented the apoptosis-induction ability of the D-gal/LPS