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. 2021 Feb 26;11:145. doi: 10.1038/s41398-021-01266-1

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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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — RAW264.7 cells (n = 5–10/grp) were treated with Pam3Cys (10 µg/ml; 30 min) (A), imiquimod (IMQ; 3 µg/ml; 24 h) (B), or Poly(I:C) (25 µg/ml; 24 h) (C) with or without 3α,5α-THP (1 µM). Cells were harvested at 24 h after treatment initiation and examined for the expression of MyD88-dependent (A, B) and TRIF-dependent (C) signal activation. A Pam3Cys caused a significant increase in the levels of TRAF6 (n = 8/grp), pERK1/2 (n = 10/grp), pCREB (n = 10/grp), pATF2 (n = 10/grp), and TNF-α (n = 5/grp) relative to vehicle control (CTL), and these increases were completely blocked by 3α,5α-THP (One-way ANOVA, Tukey’s post hoc test: *p < 0.05; **p < 0.01). B IMQ caused a significant increase in the levels of pIRF7 (n = 9/grp) and TNF-α (n = 5/grp) relative to CTL, and these increases were completely blocked by 3α,5α-THP (One-way ANOVA, Tukey’s post hoc test: *p < 0.05, **p < 0.01, ***p < 0.001). C Poly(I:C) significantly increased the levels of pIRF3 (n = 5/grp), IP-10 (n = 6/grp), and TNF-α (n = 5/grp) relative to CTL (One-way ANOVA, Tukey’s post hoc test: *p < 0.05). The increases of pIRF3, IP-10, and TNF-α were not inhibited by 3α,5α-THP (One-way ANOVA, Tukey’s post hoc test: p > 0.05). D 3α,5α-THP does not target the non-activated TLR signals. RAW264.7 cells untreated with TLR agonist but exposed to vehicle or treated with 3α,5α-THP (1 µM) were harvested after 24 h. The levels of TRAF6 (n = 6/grp), pERK1/2 (n = 6/grp), pCREB (n = 6/grp), pATF2 (n = 6/grp), TNF-α (n = 6/grp), pIRF7 (n = 6/grp), IP-10 (n = 6/grp), and pIRF3 (n = 6/grp) were similar in the 3α,5α-THP-treated and untreated cells (t-test, p > 0.05). The data indicate that 3α,5α-THP specifically targets only the activated TLR signal.