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

Figure 3 Increase in the formation of bile ducts and ductular structure in hepatic STAT3 deficient liver. A: Hematoxylin and eosin staining images of representative areas around portal vein (PV) and central vein (CV) of control and STAT3^Δhep livers following treatment with TAA for 16 wk. TAA treatment caused bile ducts/ductular formation (arrow). B: Immunohistochemistry staining for keratin 19 (KRT19) in control and STAT3^Δhep livers following TAA treatment for 16 wk. Original magnification × 200. C and D: The number of KRT19-positive bile ducts/ductules around PV and CV. To quantify the number of bile ducts/ductules around PV and CV, we observed three different samples per group using 20 × objective lens, imaged five randomly selected cross-sectional veins in the center of field, and calculated the average value after counting the bile duct/ductule number in the total area of the image. Values represent means ± SE of the mean. ^bP < 0.01 [(C) P = 0.00272, (D) P = 0.00187] vs control. TAA: Thioacetamide.