Eicosanoid profiles in an arthritis model : Effects of a soluble epoxide hydrolase inhibitor
Copyright © 2023 Elsevier B.V. All rights reserved..
Rheumatoid arthritis is a common systemic inflammatory autoimmune disease characterized by damage to joints, inflammation and pain. It is driven by an increase of inflammatory cytokines and lipids mediators such as prostaglandins. Epoxides of polyunsaturated fatty acids (PUFAs) are lipid chemical mediators in a group of regulatory compounds termed eicosanoids. These epoxy fatty acids (EpFA) have resolutive functions but are rapidly metabolized by the soluble epoxide hydrolase enzyme (sEH) into the corresponding diols. The pharmacological inhibition of sEH stabilizes EpFA from hydrolysis, improving their half-lives and biological effects. These anti-inflammatory EpFA, are analgesic in neuropathic and inflammatory pain conditions. Nonetheless, inhibition of sEH on arthritis and the resulting effects on eicosanoids profiles are little explored despite the physiological importance. In this study, we investigated the effect of sEH inhibition on collagen-induced arthritis (CIA) and its impact on the plasma eicosanoid profile. We measured the eicosanoid metabolites by LC-MS/MS-based lipidomic analysis. The treatment with a sEH inhibitor significantly modulated 11 out of 69 eicosanoids, including increased epoxides 12(13)-EpODE, 12(13)-EpOME, 13-oxo-ODE, 15-HEPE, 20-COOH-LTB4 and decreases several diols 15,6-DiHODE, 12,13-DiHOME, 14,15-DiHETrE, 5,6-DiHETrE and 16,17-DiHDPE. Overall the inhibition of sEH in the rheumatoid arthritis model enhanced epoxides generally considered anti-inflammatory or resolutive mediators and decreased several diols with inflammatory features. These findings support the hypothesis that inhibiting the sEH increases systemic EpFA levels, advancing the understanding of the impact of these lipid mediators as therapeutical targets.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:1869 |
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| Enthalten in: |
Biochimica et biophysica acta. Molecular and cell biology of lipids - 1869(2024), 2 vom: 28. Feb., Seite 159432 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Trindade-da-Silva, Carlos Antonio [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 26.01.2024 Date Revised 27.02.2024 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.bbalip.2023.159432 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM364760028 |
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| 245 | 1 | 0 | |a Eicosanoid profiles in an arthritis model |b Effects of a soluble epoxide hydrolase inhibitor |
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| 500 | |a Date Revised 27.02.2024 | ||
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| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2023 Elsevier B.V. All rights reserved. | ||
| 520 | |a Rheumatoid arthritis is a common systemic inflammatory autoimmune disease characterized by damage to joints, inflammation and pain. It is driven by an increase of inflammatory cytokines and lipids mediators such as prostaglandins. Epoxides of polyunsaturated fatty acids (PUFAs) are lipid chemical mediators in a group of regulatory compounds termed eicosanoids. These epoxy fatty acids (EpFA) have resolutive functions but are rapidly metabolized by the soluble epoxide hydrolase enzyme (sEH) into the corresponding diols. The pharmacological inhibition of sEH stabilizes EpFA from hydrolysis, improving their half-lives and biological effects. These anti-inflammatory EpFA, are analgesic in neuropathic and inflammatory pain conditions. Nonetheless, inhibition of sEH on arthritis and the resulting effects on eicosanoids profiles are little explored despite the physiological importance. In this study, we investigated the effect of sEH inhibition on collagen-induced arthritis (CIA) and its impact on the plasma eicosanoid profile. We measured the eicosanoid metabolites by LC-MS/MS-based lipidomic analysis. The treatment with a sEH inhibitor significantly modulated 11 out of 69 eicosanoids, including increased epoxides 12(13)-EpODE, 12(13)-EpOME, 13-oxo-ODE, 15-HEPE, 20-COOH-LTB4 and decreases several diols 15,6-DiHODE, 12,13-DiHOME, 14,15-DiHETrE, 5,6-DiHETrE and 16,17-DiHDPE. Overall the inhibition of sEH in the rheumatoid arthritis model enhanced epoxides generally considered anti-inflammatory or resolutive mediators and decreased several diols with inflammatory features. These findings support the hypothesis that inhibiting the sEH increases systemic EpFA levels, advancing the understanding of the impact of these lipid mediators as therapeutical targets | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, N.I.H., Extramural | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Diols | |
| 650 | 4 | |a Inflammation | |
| 650 | 4 | |a Lipidomics | |
| 650 | 4 | |a Rheumatoid arthritis | |
| 650 | 4 | |a Soluble epoxide hydrolase | |
| 650 | 7 | |a Epoxide Hydrolases |2 NLM | |
| 650 | 7 | |a EC 3.3.2.- |2 NLM | |
| 650 | 7 | |a Fatty Acids |2 NLM | |
| 650 | 7 | |a Eicosanoids |2 NLM | |
| 650 | 7 | |a Anti-Inflammatory Agents |2 NLM | |
| 650 | 7 | |a Epoxy Compounds |2 NLM | |
| 700 | 1 | |a Yang, Jun |e verfasserin |4 aut | |
| 700 | 1 | |a Fonseca, Flavia |e verfasserin |4 aut | |
| 700 | 1 | |a Pham, Hoang |e verfasserin |4 aut | |
| 700 | 1 | |a Napimoga, Marcelo Henrique |e verfasserin |4 aut | |
| 700 | 1 | |a Abdalla, Henrique Ballassini |e verfasserin |4 aut | |
| 700 | 1 | |a Aver, Geanpaolo |e verfasserin |4 aut | |
| 700 | 1 | |a De Oliveira, Márcio José Alves |e verfasserin |4 aut | |
| 700 | 1 | |a Hammock, Bruce D |e verfasserin |4 aut | |
| 700 | 1 | |a Clemente-Napimoga, Juliana Trindade |e verfasserin |4 aut | |
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