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. 2019 Jul 12;41(2):159–170. doi: 10.1093/carcin/bgz132

Figure 4.

Figure 4.

TFA-rich diet drives fibrogenesis and DR in HCVcpTg mice. (A) Representative photomicrographs of liver section stained with Azan-Mallory method. Bar = 100 μm. (B) Hepatic hydroxyproline contents. (C) Hepatic mRNA levels of genes related to fibrogenesis were quantified by qPCR, normalized to those of 18S ribosomal RNA and expressed as values relative to HCVcpTg mice fed a control diet. (D) Immunoblot analysis of αSMA, connective tissue growth factor and osteopontin. Whole-liver homogenates (60–80 μg of protein) were loaded into each well and the band of β-actin was used as a loading control. Band intensities were measured densitometrically, normalized to those of β-actin and expressed as values relative to control diet-treated HCVcpTg mice. Results were obtained from two independent immunoblot experiments and representative blots were shown. (E) Immunohistochemical staining for CK19. Proliferation of CK19-positive biliary ducts was observed only in TFA-rich diet-treated HCVcpTg mice. Bar = 40 μm. (F) Hepatic mRNA levels of genes involved in DR and hepatocyte regeneration were quantified by qPCR, normalized to those of 18S ribosomal RNA and expressed as values relative to control-diet fed HCVcpTg mice. Data are expressed as mean ± SEM. *P < 0.05 and **P < 0.01 between control diet-fed and TFA-rich diet-fed HCVcpTg mice. Con, control diet-fed HCVcpTg mice; TFA, TFA-rich diet-fed HCVcpTg mice.