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. 2020 Feb 19;10:2947. doi: 10.1038/s41598-020-59716-7

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© The Author(s) 2020

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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Narciclasine inhibited the expression of S100A8 and S100A9 in the livers of septic neonatal rats. The neonatal rats were subjected to E. coli sepsis and narciclasine (NC, 0.1, 1 and 3 mg/kg) was administered 1 hour after sepsis induction. Livers were collected 12 hours after sepsis induction. (a) The expression of S100A8 and S100A9 in the livers was determined by Immunohistochemistry. Amplification x400. (b) The protein expression of S100A8 and S100A9 in the liver was determined by western blot. The relative levels of (c) S100A8 vs β-actin, (d) S100A9 vs β-actin were determined by densitometry. The mRNA expression of (e) S100A8 and (f) S100A9 in the liver was determined by quantitative real time PCR. Data were expressed as mean ± SEM of three independent experiments and compared using ANOVA. (c,d) ***P < 0.001, compared with normal control group; ^#P < 0.05, ^##P < 0.01, ^###P < 0.001, compared with untreated sepsis group. (e,f) ^###P < 0.001, compared with sham/control group; **P < 0.01, ***P < 0.001, compared with untreated sepsis group.