Adiponectin deficiency exacerbates lipopolysaccharide/D-galactosamine-induced liver injury in mice

Figure 1 GalN/LPS induced changes in mice. A: Survival rate (n = 10); B: Plasma ALT (mean ± SE, n = 6). ^aP < 0.05, ^bP < 0.01, vs WT; C: Histology of the liver. Massive liver injury in adiponectin-/- mice. (Hematoxylin-eosin × 100); D: Large numbers of apoptotic hepatocytes in adiponectin-/- mice (TUNEL × 100). Scale bar = 400 μm. ^aP < 0.05, vs WT mice.

Figure 2 Plasma concentrations of TNF-α, IL-10 and IFN-γ in mice after GalN/LPS administration. (mean ± SE, n = 6). ^aP < 0.05, ^bP < 0.01, vs WT.

Figure 3 TNF-α, IL-10 and IFN-γ in the liver (A-C) of mice following GalN/LPS administration. (mean ± SE, n = 6). ^aP < 0.05, ^bP < 0.01, vs WT (Scheffé’s test).

Figure 4 The expressions of adipoR1 and AdipoR2 in Kupffer cells (A). Effect of adiponectin on TNF-α, IL-10 and IFN-γ production by LPS-stimulated Kupffer cells in vitro (B-D). Pre-treated with or without adiponectin (10 mg/L) for 24 h followed by the stimulation with LPS (10 mg/L). TNF-α, IL-10 and IFN-γ mRNA expression in Kupffer cells after LPS stimulation (E-G). (mean ± SE, n = 6). ^aP < 0.05, ^bP < 0.01 (Scheffé’s test).