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. 2021 Dec 20;19:429. doi: 10.1186/s12951-021-01175-x

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© The Author(s) 2021

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. 2 — Lipo-RSV promoted macrophage repolarization from M1- to M2-like phenotype. A Flow cytometry analysis of the M1-like subset (F4/80⁺CD86⁺) and M2-like subset (F4/80⁺CD206⁺). Statistical analysis of the percent of B M1Φ (F4/80⁺CD206⁺) or C M2Φ (F4/80⁺CD86⁺).The mRNA leavel of D–F M2-related markers (CD206, Arg-1 and Chil3), and G–I M1 macrophage markers (CD86, iNOS and CCR7) in the activated macrophages. J Lipo-RSV upregulate CD206 and downregulate iNOS and CD86 protein. K Lipo-RSV promoted the phosphorylation of STAT3 and inhibited the phosphorylation of STAT1. Data are presented as mean ± SD (n = 3); ns, no significance, **P < 0.01, ***P < 0.001, ****P < 0.0001. R: RSV (15 μM); LR: Lipo-RSV (equal to 15 μM RSV)