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. 2018 May 29;8:8319. doi: 10.1038/s41598-018-26637-5

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© The Author(s) 2018

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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Diabetic mice were protected by the administration of HMGB1 A Box. (a) Diabetic mice given saline developed significant albuminuria versus non-diabetic mice (UACR: 165.3 ± 56.3 versus 51.1 ± 9.7 mg/mmol), whilst A Box treated-diabetic mice were protected with significantly less production of albuminuria (110.8 ± 29.6 mg/mmol). (b–h) WT diabetic mice demonstrated significant glomerular injury including glomerular hypertrophy, glomerular hypercellularity, glomerular mesangial matrix expansion, podocin injury, WT1⁺ podocyte injury, interstitial fibrosis and macrophage accumulation compared to non-diabetic controls, but changes were attenuated by A Box treatment. (i) mRNA expression of cytokine (TGF-β and CXCL10), chemokine (CCL2) and pro-fibrotic (fibronectin) genes were significantly up-regulated in saline-treated diabetic kidney versus non-diabetic controls but significantly attenuated in diabetic mice treated with A Box versus saline-treated diabetic mice. Data are presented as mean ± SD; *p < 0.05, **p < 0.01, ***p < 0.001.