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. 2013 Dec 10;19(17):1983–1998. doi: 10.1089/ars.2012.4946

FIG. 1.

FIG. 1.

Analysis of the expression of PRDX mRNA in the mice. (A) RT-PCR showed that the liver of WT and Tg mice expressed endogenous mPRDX4. WT mice did not express hPRDX4. The expression of hPRDX4 was significantly greater compared with mPRDX4 in both control (n=5 mice per group) and HFrD+STZ (n=10 mice per group) Tg mice. In Tg mice, hPRDX4 expression was also significantly greater in HFrD+STZ mice than in control mice. (B) Real-time RT-PCR confirmed that hPRDX4 expression was markedly increased in HFrD+STZ Tg mice (n=10 mice per group) (***p<0.0001). (C) Expression levels of mPRDX1, 2, 3, 5, and 6 were not significantly different between WT and Tg mice (HFrD+STZ, n=10 mice per group). However, hepatic expression of endogenous mPRDX4 was significantly higher in Tg mice than in WT mice (***p<0.0001). Values are means±SE in B–C and were normalized for 18S rRNA expression (real-time RT-PCR) or GAPDH expression (RT-PCR) in (A–C). HFrD, high-fructose diet; hPRDX4, human peroxiredoxin 4; mPRDX4, mouse peroxiredoxin 4; RT-PCR, reverse transcriptase–polymerase chain reaction; STZ, streptozotocin; Tg, hPRDX4 transgenic; WT, wild type; GAPDH, glyceraldehydes 3-phosphate dehydrogenase.