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. 2023 Jan 19;21:21. doi: 10.1186/s12951-023-01770-0

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© The Author(s) 2023

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 — Schematic representation of the preparation of D-CeO₂ and its anti-inflammatory/anti-fibrotic mechanism. D-CeO₂ was synthesized by the precipitation method, and the color of the solution changed from yellow to dark brown during the synthetic process. Orally administered of D-CeO₂ to mice by chitosan/alginate hydrogel. In the site of colitis, the hydrogel collapsed to release D-CeO₂. On the one hand, D-CeO₂ played a role in promoting the repair of damaged tissues by scavenging ROS. On the other hand, it alleviated fibrosis by decreasing the levels of fibrosis-related cytokines