STAT3 deficiency prevents hepatocarcinogenesis and promotes biliary proliferation in thioacetamide-induced liver injury

Figure 1 Establishment of hepatic-STAT3 deficient (STAT3^Δhep) mice. Hepatic-STAT3 deficiency enhanced thioacetamide-induced liver injury. A: The exon 21 of STAT3 was flanked by two identically oriented loxP sites (STAT3^flox/flox). To disrupt hepatic-STAT3 gene, STAT3^flox/flox mice were crossed with mice carrying albumin promoter-driven Cre transgene (Alb-Cre). Deficiency of hepatic-STAT3 protein was confirmed by immunoblotting analysis. B: Representative hematoxylin and eosin (H&E) staining images of control and STAT3^Δhep livers with TAA treatment for 16 wk. Hepatic-STAT3 deficiency accelerated inflammation cells infiltration and hepatocytes necrosis. C: Quantification of necrotic hepatocytes. Necrotic hepatocyte was identified with the eosinophilic/vacuolated cytoplasm and nuclear destruction such as karyolysis or Pyknosis. Values represent means ± SE of the mean. ^bP < 0.01 (P = 0.000269) vs control. D: Representative Azan staining of control and STAT3Δhep livers with TAA treatment for 16 wk. E: Quantification of the ratio of fibrosis area to the total area in control and STAT3^Δhep livers. Values represent means ± SE of the mean. ^bP < 0.01 (P = 0.00235) vs control. TAA: Thioacetamide.