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. 2024 May 15;14:11160. doi: 10.1038/s41598-024-61777-x

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© The Author(s) 2024

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 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/.

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SLC16A10 mediates the anti-inflammatory effect of miR-21-5p. (A) A549 cells were co-transfected with miR-21-5p inhibitor and si-SLC16A10, and the mRNA levels of SLC16A10, IL-1β and TNF-α were measured by RT-qPCR in six groups. including the control group, LPS, LPS + NC inhibitor, LPS + miR-21-5p inhibitor, LPS + miR-21-5p inhibitor + NC siRNA, LPS + miR-21-5p inhibitor + si-SLC16A10 (n = 3). (B) Western blot further verified the expression levels of SLC16A10, IL-1β and TNF-α in six groups. (C) Quantification analysis of protein expression levels of SLC16A10, IL-1β and TNF-α (n = 3). All data are shown as the mean ± SEM. ****P ≤ 0.0001, ***P ≤ 0.001, **P < 0.01, *P < 0.05; NS, not significant (P > 0.05).