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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 attenuated glomerular heparanase expression in DN mice (n = 5). (A) The glomerular heparanase expression was determined by immunofluorescence staining using the heparanase primary antibody (Ab85543) detecting 65 kD precursor as well as the 50 kD and 8 kD subunits of heparanase followed by rhodamine conjugated secondary antibody. (B) The heparanase primary antibody (MBS71555) followed by FITC conjugated secondary antibody was used to show 65 kD heparanase. 1:Control; 2:DN; 3:LHPS; 4:HHPS. (C,D) Quantification was performed by NIH Image software and shown in columns. (E) The columns showed the amount of heparanase mRNA levels relative to β-actin. Data are presented as mean ± SD. P < 0.05 is statistically significant. ^aIndicates significant vs. Control, ^bindicates significant vs. DN.