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. 2022 Nov 3;20:469. doi: 10.1186/s12951-022-01681-6

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© The Author(s) 2022

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. 4 — CDs inhibited IL-1β-induced oxidative stress. A Intracellular ROS in chondrocytes with different treatment. Scar bar: 100 μm. B The elevated level of iNOS and COX-2 in IL-1β-induced chondrocytes was rescued by CDs treatment. C Western blot assay indicated CDs could effectively inhibit iNOS and COX-2 expression. D Immunostaining assay showed the dysregulation of iNOS and COX-2 was rescued by CDs treatment. Scar bar: 20 μm. E The restorative effect of CDs on ATP production in IL-1β-stimulated chondrocytes. *p < 0.05; **p < 0.01; ***p < 0.001