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. 2017 Jun 27;7:4261. doi: 10.1038/s41598-017-00686-8

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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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PLK2 knockdown suppressed diabetes-induced apoptosis and inflammatory responses in rats. Diabetic rats (n = 3) were analyzed 24 h after shPLK2 lentiviral injection. (A–C) The urinary levels of creatinine, nitrogen and protein in diabetic rats were measured by biochemical assay. (D) Glomeruli of diabetic rats with H&E staining, PLK2 immunohistochemistry, TUNEL assay, and Nephrin staining. (E,F) Quantitative analysis and representative images of western blot. PLK2 was up-regulated in diabetic rats. Expression of apoptosis-associated markers including SIRT5, Bcl-2/Bax, p53 and cleaved caspase-3 in rats was measured. (G) Inflammatory factors TNF-α, IL-6, IL-1β, COX-2 and CXCL1 content in rats. *P < 0.05, **P < 0.01.