期刊
EUROPEAN JOURNAL OF PAIN
卷 19, 期 1, 页码 111-122出版社
WILEY
DOI: 10.1002/ejp.528
关键词
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资金
- Fundacion Mutua Madrilena
- INNPACTO (Ministerio de Ciencia e Innovacion) [IPT-010000-2010-016]
- Consorcio 'Dendria-Draconis Pharma S.L.' (Centro para el Desarrollo Tecnologico Industrial)
- Instituto de Salud Carlos III [PI11/00592]
- [BIO2010-21132]
BackgroundRecently, fatty acids have been shown to modulate sensory function in animal models of neuropathic pain. In this study, the antinociceptive effect of 2-hydroxyoleic acid (2-OHOA) was assessed following spared nerve injury (SNI) with reflex and cerebrally mediated behavioural responses. MethodsInitial antinociceptive behavioural screening of daily administration of 2-OHOA (400mg/kg, p.o.) was assessed in Wistar rats by measuring hindlimb reflex hypersensitivity to von Frey and thermal plate stimulation up to 7 days after SNI, while its modulatory effect on lumbar spinal dorsal horn microglia reactivity was assessed with OX-42 immunohistochemistry. In vitro the effect of 2-OHOA (120M) on cyclooxygenase protein expression (COX-2/COX-1 ratio) in lipopolysaccharide-activated macrophage cells was tested with Western blot analysis. Finally, the effects of 2-OHOA treatment on the place escape aversion paradigm (PEAP) and the open-field-induced anxiety test were tested at 21 days following nerve injury compared with vehicle-treated sham and pregabalin-SNI (30mg/kg, p.o.) control groups. ResultsOral 2-OHOA significantly reduced ipsilateral mechanical and thermal hypersensitivity up to 7 days after SNI. Additionally 2-OHOA decreased the COX-2/COX-1 ratio in lipopolysaccharide-activated macrophage cells and OX-42 expression within the ipsilateral lumbar spinal dorsal horn 7 days after SNI. 2-OHOA significantly restored inner-zone exploration in the open-field test compared with the vehicle-treated sham group at 21 days after SNI. ConclusionsOral administration of the modified omega 9 fatty acid, 2-OHOA, mediates antinociception and prevents open-field-induced anxiety in the SNI model in Wistar rats, which is mediated by an inhibition of spinal dorsal horn microglia activation.
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