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. 2018 Feb 12;8:3052. doi: 10.1038/s41598-017-13139-z

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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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C23 attenuates AKI after CLP. Renal function and injury was evaluated in serum and kidney tissue samples collected at 20 h after CLP. (A) The serum creatinine was significantly elevated in the vehicle group, and there was a trend for lower levels in C23-treated mice (C23 v. vehicle, p = 0.052). (B) The BUN was significantly elevated in the vehicle group, and significantly reduced in C23-treated mice. (C) NGAL gene expression was significantly elevated in the vehicle group, and significantly reduced in C23-treated mice. (D) KIM-1 gene expression was significantly elevated in the vehicle group, and significantly reduced in C23-treated mice. Data are presented as means ± SE. Number of animals in each group: sham n = 5, vehicle n = 7, C23 n = 6. *p < 0.05 vs. sham, ^#p < 0.05 vs. vehicle; one-way ANOVA followed by Student-Newman-Keuls test.