<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Dong L</submitter><funding>Project supported by Hunan Provincial Natural Science Foundation of China</funding><funding>NIEHS NIH HHS</funding><funding>High School Innovation Fund of Hunan province</funding><funding>National Natural Science Foundation of China</funding><funding>Open-End Fund for the Valuable and Precision Instruments of Central South University</funding><pagination>13-20</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7990107</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>40(1)</volume><pubmed_abstract>Triggering receptors expressed on myeloid cell-1 (TREM-1) is a superimmunoglobulin receptor expressed on myeloid cells. TREM-1 amplifies the inflammatory response. Epoxyeicosatrienoic acids (EETs), the metabolites of arachidonic acid derived from the cytochrome P450 enzyme, have anti-inflammatory properties. However, the effects of EETs on TREM-1 expression under inflammatory stimulation remain unclear. Therefore, inhibition of soluble epoxide hydrolase (sEH) with a highly selective inhibitor [1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea, TPPU] was used to stabilize EETs. LPS was intratracheally injected into mice to induce pulmonary inflammation, after TPPU treatment for 3 h. Histological examination showed TPPU treatment-alleviated LPS-induced pulmonary inflammation. TPPU decreased TREM-1 expression, but not DAP12 or MyD88 expression. Murine peritoneal macrophages were challenged with LPS in vitro. We found that TPPU reduced LPS-induced TREM-1 expression in a dose-dependent manner, but not DAP12 or MyD88 expression. TPPU also decreased downstream signal from TREM-1, reducing pro-inflammatory cytokine TNF-α and IL-1β mRNA expression. Furthermore, TPPU treatment inhibited IkB degradation in vivo and in vitro. Our results indicate that the inhibition of sEH suppresses LPS-induced TREM-1 expression and inflammation via inhibiting NF-kB activation in murine macrophage.</pubmed_abstract><journal>Inflammation</journal><pubmed_title>Soluble Epoxide Hydrolase Inhibitor Suppresses the Expression of Triggering Receptor Expressed on Myeloid Cells-1 by Inhibiting NF-kB Activation in Murine Macrophage.</pubmed_title><pmcid>PMC7990107</pmcid><funding_grant_id>14JJ2040</funding_grant_id><funding_grant_id>P42 ES004699</funding_grant_id><funding_grant_id>81670014</funding_grant_id><funding_grant_id>81500065</funding_grant_id><funding_grant_id>15K140</funding_grant_id><funding_grant_id>R35 ES030443</funding_grant_id><funding_grant_id>CSUCZ201632</funding_grant_id><pubmed_authors>Guan CX</pubmed_authors><pubmed_authors>Zhu ZQ</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Hammcok BD</pubmed_authors><pubmed_authors>Duan JX</pubmed_authors><pubmed_authors>Dong L</pubmed_authors><pubmed_authors>Li P</pubmed_authors><pubmed_authors>Zhou Y</pubmed_authors><pubmed_authors>Liu T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Soluble Epoxide Hydrolase Inhibitor Suppresses the Expression of Triggering Receptor Expressed on Myeloid Cells-1 by Inhibiting NF-kB Activation in Murine Macrophage.</name><description>Triggering receptors expressed on myeloid cell-1 (TREM-1) is a superimmunoglobulin receptor expressed on myeloid cells. TREM-1 amplifies the inflammatory response. Epoxyeicosatrienoic acids (EETs), the metabolites of arachidonic acid derived from the cytochrome P450 enzyme, have anti-inflammatory properties. However, the effects of EETs on TREM-1 expression under inflammatory stimulation remain unclear. Therefore, inhibition of soluble epoxide hydrolase (sEH) with a highly selective inhibitor [1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea, TPPU] was used to stabilize EETs. LPS was intratracheally injected into mice to induce pulmonary inflammation, after TPPU treatment for 3 h. Histological examination showed TPPU treatment-alleviated LPS-induced pulmonary inflammation. TPPU decreased TREM-1 expression, but not DAP12 or MyD88 expression. Murine peritoneal macrophages were challenged with LPS in vitro. We found that TPPU reduced LPS-induced TREM-1 expression in a dose-dependent manner, but not DAP12 or MyD88 expression. TPPU also decreased downstream signal from TREM-1, reducing pro-inflammatory cytokine TNF-α and IL-1β mRNA expression. Furthermore, TPPU treatment inhibited IkB degradation in vivo and in vitro. Our results indicate that the inhibition of sEH suppresses LPS-induced TREM-1 expression and inflammation via inhibiting NF-kB activation in murine macrophage.</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Feb</publication><modification>2025-04-04T12:32:55.61Z</modification><creation>2025-04-04T12:32:55.61Z</creation></dates><accession>S-EPMC7990107</accession><cross_references><pubmed>27696333</pubmed><doi>10.1007/s10753-016-0448-6</doi></cross_references></HashMap>