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. 2019 Jun 29;16:132. doi: 10.1186/s12974-019-1507-3

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 9 — Conceptual summary. HDAC5 was activated upon CFA insult, resulting in reduced expression of AcH3 and AcH4 on Lxrβ promoter, which contributed to the reduction of LXRβ expression. SAHA treatment sequestered HDACs that promoted AcH3 expression on Lxrβ promoter and LXRβ expression. LXRβ activation by GW3965 was able to reverse the nuclear translocation of p65 and p50, reduce the phosphorylation of mitogen-activated protein kinases (MAPKs) signaling pathways, regulate the TNF-α expression, and modulate the enhanced excitatory synaptic transmission in CFA-induced chronic inflammatory pain