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. 2021 Oct 30;18:249. doi: 10.1186/s12974-021-02231-x

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — RSL3 inhibits LPS-induced proinflammatory cytokine production of microglia and PMs. a qRT-PCR analysis of TNF, IL-6, and IL-1b mRNA levels in LPS (100 ng/ML)-stimulated PMs subjected to different doses of RSL3 treatment for 4 h. b ELISA of TNFα, IL-6, and IL-1β in supernatants of LPS-stimulated PMs subjected to different doses of RSL3 treatment for 8 h. c qRT-PCR analysis of TNF, IL-6, and IL-1b mRNA levels in LPS (100 ng/ML)-stimulated BV2 cells subjected to different doses of RSL3 treatment for 4 h. d ELISA of TNFα, IL-6, and IL-1β in supernatants of LPS-stimulated BV2 cells subjected to different doses of RSL3 treatment for 8 h. The data are means ± SD; for all panels, *P < 0.05, **P < 0.01, ***P < 0.001 by one-way-ANOVA analysis followed by Dunnett test. n.s., no significant. The data are combined from three independent experiments