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. 2024 Aug 22;25:321. doi: 10.1186/s12931-024-02951-7

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 7 — 1,25(OH)₂D₃ reduced the formation of inflammatory cytokines in PM stimulated BEAS-2B cultures. Culture supernatants were collected 24 h after PM stimulation without or with 1,25(OH)₂D₃ pretreatment, and the concentrations of IL-6 and MCP-1 were measured. Concentration-dependent increases in IL-6 (A) and MCP-1 (B) were observed; however, addition of 1,25(OH)₂D₃ reduced the release of inflammatory cytokines IL-6 (C) and MCP-1 (D). (E-G) In addition, 1,25(OH)₂D₃ alleviated the generation of certain inflammatory cytokines triggered by antimycin A, which disrupts mitochondria with reduced membrane potential. Data were mean ± SD of three independent experiments. ^***P < 0.001, ^**P < 0.01 and ^*P < 0.05 as compared with untreated cells (control)