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. 2017 Jul 25;7:6413. doi: 10.1038/s41598-017-06844-2

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© The Author(s) 2017

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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Hyperoside pre-treatment alleviated renal cortex oxidative stress and heparanase protein expression in DN mice (n = 15). (A) The levels of ROS-related end product MDA in renal cortex were measured among indicated groups. (B–D) The activity of ROS-related enzymes SOD, CAT and XO was measured among indicated groups. (E,F) Renal cortex heparanase protein expression was detected by western blot analysis and the columns showed the relative quatification of heparanase protein levels normalized to β-actin. Control: Normal mice; DN: DM mice were treated with vehicle solution for four weeks; LHPS and HHPS: DM mice were treated with 10 or 30 mg/kg/d hyperoside for four weeks respectively from two weeks after DM establishment. Data are presented as mean ± SD. P < 0.05 is statistically significant. ^aIndicates significant vs. Control, ^bindicates significant vs. DN.