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. Author manuscript; available in PMC: 2018 Dec 28.
Published in final edited form as: Glycoconj J. 2016 Jun 18;33(6):927–936. doi: 10.1007/s10719-016-9703-1

Fig. 3.

Fig. 3

Changes in oxidative stress a–e mRNA expression of genes involved in ROS generation (Aox, Cyp4a, and Nox2) and elimination (Cat and Sod1) were measured in 3- and 16-month-old HCVcpTg and non-Tg mice. Levels of mRNA were analyzed by qPCR and normalized to those of Gapdh mRNA. Data are shown as the fold changes to those of 3-month-old HCVcpTg mice and expressed as the mean ± SD. f Hepatic content of MDA, a representative lipid peroxidation maker. Data are expressed as the mean ± SD (n = 6 for 3-month-old HCVcpTg mice; n = 6 for 16-month-old HCVcpTg mice without HCC; n = 5 for 16month-old HCVcpTg mice with HCC; n = 6 for MK886-treated 16month-old HCVcpTg mice without HCC; n = 4 for MK886-treated 16month-old HCVcpTg mice with HCC; n = 4 for 3-month-old non-Tg mice; and n = 4 for 16-month-old non-Tg mice). Closed bars indicate non-tumor liver samples. Open bars indicate liver cancer samples. HCVcp, HCV core protein; HCC, hepatocellular carcinomas; Aox, acylCoA oxidase; Cyp4a, cytochrome P450 4 A; Nox2, NADPH oxidase subunit 2; Cat, catalase; Sod1, superoxide dismutase 1. * p < 0.05, ** p < 0.01; comparison among sample groups for the Tg or non-Tg mice. # p < 0.05; compared with non-treated age-matched Tg mice without HCC. §p < 0.05; compared with non-treated age-matched Tg mice with HCC