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. Author manuscript; available in PMC: 2014 Mar 27.
Published in final edited form as: Liver Int. 2011 Mar 21;31(7):950–963. doi: 10.1111/j.1478-3231.2011.02514.x

Fig. 2.

Fig. 2

Characteristics of liver injury. Immunohistochemistry of cytokeratin 8 and 18 staining (× 100) of liver derived from Long–Evans (LE) (A) and Fischer (B) rats. In the LE strain (inset × 400), there was macro- and microsteatosis, hepatocyte degeneration (large arrow) and foci of inflammation (small arrows) (C) Body weight of thioacetamide-treated LE rats compared with control. (D) Triglyceride levels (TG) of thioacetamide or saline-treated LE rats, *P < 0.05. Significantly less IG deposition in the thioacetamide-treated group was observed. (E) Serum alanine aminotransferase (ALT) levels in thioacetamide and control LE rats. H&E staining of control (F) and thioacetamide-treated (G) rat livers illustrating hepatocyte necrosis and cell drop out as well as lobular disarray (× 100). Cytokeratin 8 and 18 immunostaining of (H) control and thioacetamide-treated (I) rat liver demonstrate reduced staining in degenerating hepatocytes and lesser degree of immunoreactivity in severely steatotic hepatocytes of ethanol-treated LE rats (A and B; × 200). (J) Represents Oil Red-O staining of thioacetamide-treated rat liver demonstrating strikingly lower lipid accumulation compared with alcoholic liver disease (ALD) (see Fig. 1E; × 200). (K) Trichrome staining of thioacetamide-treated rat liver demonstrating the presence of cirrhosis in addition to severe liver injury (× 10).