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. 2022 Mar 19;12:4754. doi: 10.1038/s41598-022-08398-4

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© The Author(s) 2022

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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Mesenchymal stem cell conditioned media inhibited the LPS-induced expression of pro-inflammatory enzymes. LPS stimulation effectively upregulated the production of COX-2 and iNOS, which was reduced by pretreatment with MSC-CM (A). Representative western blots of COX-2 (B) and iNOS (C) expression in LPS-stimulated RAW264.7 cells with or without MSC-CM treatment for 24 h; quantitative data representing the average values of three separate experiments. Fluorescence images (× 200) of RAW264.7 cells immunostained for COX-2 (green) and DAPI (blue) (D) as well as iNOS (green) and DAPI (blue) (E). LPS treatment was performed for 6 h after pretreatment with MSC-CM. The results are representative of three separate experiments (^*P < 0.05, ^**P < 0.01 compared with LPS stimulation without MSC-CM). The Fig. 1A and D were cropped to improve the clarity and conciseness of the presentation, and the full-length blots/gels are presented in Supplementary file. MSC-CM, mesenchymal stem cell conditioned media; D1-M (CON), D1 cell media; D1-M (IL4), D1 cell media stimulated with IL4; LPS, lipopolysaccharides; COX-2, cyclooxygenase-2; iNOS, inducible nitric oxide synthase.