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. 2017 Dec 11;7:17332. doi: 10.1038/s41598-017-17427-6

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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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AaE and its active components suppress c-Fos and NFATc1 expression in RANKL-treated BMMs. BMMs were incubated with M-CSF (30 ng/mL), RANKL (50 ng/mL), and the indicated concentrations of (a) AaE and (b) artemisinin (ART), artemisinic acid (AA), or arteannuin B (AB) for 2 days. The expression levels of c-Fos and NFATc1 were examined by western blot analysis. The band intensity of each protein was densitometrically measured with TINA software and normalized to that of GAPDH as an internal control. The images are representative. (c) The mRNA expression levels of c-Fos and NFATc1 were detected using qRT-PCR and normalized to that of GAPDH. The data are expressed as the mean ± SE of triplicate experiments. ^# P < 0.01 versus BMMs without RANKL (C), ^* P < 0.05, ^** P < 0.01 versus BMMs with RANKL alone.