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. 2019 Jun 19;9:8751. doi: 10.1038/s41598-019-45347-0

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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The level of oxidative stress markers in UUO-induced PrdxV^wt and PrdxV^si mouse kidney. As one of the major mechanisms of renal fibrosis induced by UUO, the level of oxidative stress was assessed in both PrdxV^wt and PrdxV^si mouse kidneys. (a) The increased nitrotyrosine level in UUO-induced PrdxV^si kidney. The content of nitrotyrosine, as a protein oxidative marker, was analyzed by western blotting conducted with whole kidney lysates. Three major bands of different sizes were detected at 80 kDa, 50 kDa, and 35 kDa. GAPDH was used as an internal control. (b) The increased HHE level in UUO-induced PrdxV^si kidney. The content of HHE, as a lipid peroxidation marker, was analyzed by immunohistochemistry with a specific anti-HHE antibody. Image was magnified at x100, Bar = 200 μm. All values are presented as mean ± SD. Statistical significance was measured using the one-way ANOVA with the Fisher least significant difference post-test. ^§p < 0.05; PrdxV^wt vs. PrdxV^si in UUO group.