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. 2017 Aug 7;7:7393. doi: 10.1038/s41598-017-07952-9

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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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Akt is involved in HIMF-induced IL-18 production. (A) Cells were incubated with HIMF (3 nM) for indicated time intervals and cell lysates were immunoblotted with an antibody specific for phospho-Akt. (B) Cells were transfected with Akt siRNA for 24 h, and Akt protein expression was analyzed. (C) HIMF-induced IL-18 mRNA was inhibited by the Akt inhibitor or Akt siRNA. (D) Cells were pretreated for 30 min with the Akt inhibitor or transfected with Akt siRNA for 24 h, then stimulated with HIMF for 24 h, and the conditioned media was collected and examined by ELISA. (E) HIMF-induced Akt phosphorylation was inhibited by an Akt inhibitor or Akt siRNA. (F) Cells were treated with the PDK1 inhibitor or LY294002 for 30 min then stimulated with HIMF for 120 min, and phospho-Akt protein expression was analyzed. Results are expressed as the means ± SEM of four independent experiments. *p < 0.05 as compared with the control group. #p < 0.05 as compared with HIMF-treated group.