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. 2021 Feb 11;19:13. doi: 10.1186/s12964-020-00647-1

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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. 5 — Icariside I facilitates ATP/nigericin-induced NLRP3 inflammasome activation dependent on mitochondrial ROS production. a, b LPS-primed BMDMs were treated with Icariside I before stimulated with ATP, nigericin, SiO2. BMDMs were loaded with MitoSOX red mitochondrial superoxide indicator (Ex/Em: 510/580 nm). After staining and washing, flow cytometry was conducted to test mtROS production. c Confocal microscopy analysis in LPS-primed BMDMs treated with Icariside I (20 μM) and then left stimulated with ATP, followed by staining with Mitotracker red and DAPI. Data are represented as the mean ± SD from at least three biological samples. ^#p < 0.05 vs. the control group. *P < 0.05