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. 2021 May 27;11:11168. doi: 10.1038/s41598-021-90605-9

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© The Author(s) 2021

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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Vitamin D attenuates the CoCl₂-induced increase of COX-2 expression. (A,B) COX-2 expression examined by quantitative PCR and Western blot in HTR-8/SVneo cells treated with CoCl₂ in the presence or absence of 1,25(OH)₂D₃. CoCl₂-induced increase of COX-2 expression could be significantly attenuated in cells treated with 1,25(OH)₂D₃. The bar graphs show relative expression for COX-2 after normalization to β-actin expression in each sample. *P < 0.05: 1,25(OH)₂D₃ treated vs control cells. **P < 0.01: CoCl₂ alone vs control. ^#P < 0.05: 1,25(OH)₂D₃ + CoCl₂ vs CoCl₂ alone. Data are presented as mean ± SE from six independent experiments. (C) Representative imaging of immunofluorescence staining of COX-2 in HTR-8/SVneo cells treated with CoCl₂ in the presence or absence of 1,25(OH)₂D₃. Consistent with the Western blot results, 1,25(OH)₂D₃ could inhibit the CoCl₂-induced increase of COX-2 expression in placental trophoblasts.