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. 2019 Feb 15;15:1744806919830018. doi: 10.1177/1744806919830018

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© The Author(s) 2019

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 6. — TNBS-induced colitis activates the canonical TLR4 signaling pathway in DRG neurons. (a) Representative western blot gel bands for adaptor proteins MyD88 and TRIF, IL-1β, IL-6, and NF-κB in the DRG from vehicle or TNBS-treated WT and TLR4-KO mice. (b) Statistic graphs showing activation of the canonical TLR4 signaling pathway in TNBS-induced colitis (n = 6 per group). *p < 0.05; **p < 0.01; ***p < 0.001 (one-way ANOVA followed by Bonferroni’s multiple comparisons test), ^#p < 0.05; ^##p < 0.01; ^###p < 0.001 (Student’s t test). WT: wild type; TLR4: Toll-like receptor 4; KO: knockout; TNBS: 2,4,6-trinitrobenzene sulfate; GAPDH: glyceraldehyde 3-phosphate dehydrogenase; IL: interleukin; NF-κB: nuclear factor kappa B; TRIF: Toll/IL-1 receptor domain-containing adapter inducing interferon-beta; RU: response units.