Aspirin-triggered Lipoxin A4 attenuates mechanical allodynia in association with inhibiting spinal JAK2/STAT3 signaling in neuropathic pain in rats

Wang, Z.-F.; Li, Q.; Liu, S.-B.; Mi, Wen-Li; Hu, Song; Zhao, Jingang; Tian, Yu; Mao-Ying, Qi-Liang; Jiang, Jinju; Ma, Haijun; Wang, Y.-Q.; Wu, Gen-Cheng

doi:10.1016/j.neuroscience.2014.04.052

Cited by 69 publications

(53 citation statements)

References 69 publications

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“…The use of different nociceptive endpoints, animal species and route of aspirin administration may contribute to this discrepancy. Our results are consistent with recent findings of Wang et al [40] who showed that aspirin administered in the form of its endogenous mediator (aspirin-triggered Lipoxin A4) reversed mechanical allodynia in other model of peripheral neuropathy (chronic constriction injury in rats).…”

Section: Discussionsupporting

confidence: 93%

“…Evidence suggests that up-regulation of cyclooxygenase-2 (COX-2) in the peripheral nerves and dorsal root ganglia neurons, as well as, raised serum tumor necrosis factor alpha (TNF ␣ ) play an important role in the pathogenesis of painful diabetic neuropathy [18,[42][43][44]. Therefore, the antinociceptive effects of ibuprofen [18,45], aspirin [40,46], and paracetamol [21,47,48] in this type of pain could be explained by their inhibition of COX-2 and ability to decrease TNF ␣ levels. It has been recently shown that ibuprofen [49], and aspirin [50] inhibit microglial activity, which could also explain their effectiveness in diabetic neuropathy, as activated microglia may be involved in the development of diabetic neuropathy [51,52].…”

Section: Discussionmentioning

confidence: 99%

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Levetiracetam synergises with common analgesics in producing antinociception in a mouse model of painful diabetic neuropathy

Micov

Tomić

Pecikoza

et al. 2015

Pharmacological Research

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Levetiracetam synergises with common analgesics in producing antinociception in a mouse model of painful diabetic neuropathy

Micov

Tomić

Pecikoza

et al. 2015

Pharmacological Research

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“…Concentrations of AT-RvD1 and butoxy carbonyl-Phe-Leu-Phe-Leu-Phe (BOC-2), a FPR2/ALX receptor antagonist [29], were based on previous studies [13, 30]. AT-RvD1 and RvD1 have similar chemical structures; however, AT-RvD1 is more resistant to enzymatic inactivation by 15-hydroxyprostaglandin dehydrogenase (15-PGDH) [9].…”

Section: Methodsmentioning

confidence: 99%

Inhibitory effects of aspirin-triggered resolvin D1 on spinal nociceptive processing in rat pain models

Meesawatsom

Burston

Hathway

et al. 2016

J Neuroinflammation

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BackgroundHarnessing the actions of the resolvin pathways has the potential for the treatment of a wide range of conditions associated with overt inflammatory signalling. Aspirin-triggered resolvin D1 (AT-RvD1) has robust analgesic effects in behavioural models of pain; however, the potential underlying spinal neurophysiological mechanisms contributing to these inhibitory effects in vivo are yet to be determined. This study investigated the acute effects of spinal AT-RvD1 on evoked responses of spinal neurones in vivo in a model of acute inflammatory pain and chronic osteoarthritic (OA) pain and the relevance of alterations in spinal gene expression to these neurophysiological effects.MethodsPain behaviour was assessed in rats with established carrageenan-induced inflammatory or monosodium iodoacetate (MIA)-induced OA pain, and changes in spinal gene expression of resolvin receptors and relevant enzymatic pathways were examined. At timepoints of established pain behaviour, responses of deep dorsal horn wide dynamic range (WDR) neurones to transcutaneous electrical stimulation of the hind paw were recorded pre- and post direct spinal administration of AT-RvD1 (15 and 150 ng/50 μl).ResultsAT-RvD1 (15 ng/50 μl) significantly inhibited WDR neurone responses to electrical stimuli at C- (29 % inhibition) and Aδ-fibre (27 % inhibition) intensities. Both wind-up (53 %) and post-discharge (46 %) responses of WDR neurones in carrageenan-treated animals were significantly inhibited by AT-RvD1, compared to pre-drug response (p < 0.05). These effects were abolished by spinal pre-administration of a formyl peptide receptor 2 (FPR2/ALX) antagonist, butoxy carbonyl-Phe-Leu-Phe-Leu-Phe (BOC-2) (50 μg/50 μl). AT-RvD1 did not alter evoked WDR neurone responses in non-inflamed or MIA-treated rats. Electrophysiological effects in carrageenan-inflamed rats were accompanied by a significant increase in messenger RNA (mRNA) for chemerin (ChemR23) receptor and 5-lipoxygenase-activating protein (FLAP) and a decrease in 15-lipoxygenase (15-LOX) mRNA in the ipsilateral spinal cord of the carrageenan group, compared to controls.ConclusionsOur data suggest that peripheral inflammation-mediated changes in spinal FLAP expression may contribute to the novel inhibitory effects of spinal AT-RvD1 on WDR neuronal excitability, which are mediated by FPR2/ALX receptors. Inflammatory-driven changes in this pathway may offer novel targets for inflammatory pain treatment.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-016-0676-6) contains supplementary material, which is available to authorized users.

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“…Antihyperalgesic effect for LXA4 and its derivatives is very well documented in different animal models (Petri et al, 2015;Wang et al, 2014;Abdelmoaty et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

“…Specific pro-resolving mediators and pathways are operative to enact resolution including those centred on annexin A1 (AnxA1) and lipoxin A4 (LXA4) (Cash et al, 2014). Accumulating evidence from diverse animal models indicate modulatory properties for pro-resolving mediators on nociception (Pei et al, 2011;Pierretti et al, 2001) and hyperalgesia (Abdelmoaty et al, 2013;Hu et al, 2012;Huang et al, 2011), through mechanisms that involve modulation of the expression of transcriptional factors and cytokines (Liu et al, 2016;Sun et al, 2012;Wang et al, 2014). Similarly, pivotal roles for the endogenous local signals that govern resolution to impact on pain processes have already defined (for review : Serhan, 2008).…”

Section: Introductionmentioning

confidence: 99%

Hydroalcoholic crude extract of Casearia sylvestris Sw. reduces chronic post-ischemic pain by activation of pro-resolving pathways

Piovezan

Batisti

Benevides

et al. 2017

Journal of Ethnopharmacology

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Ethnopharmacological relevanceCasearia sylvestris Sw. is widely used in popular medicine to treat conditions associated with pain. Aim of the studyThe present study investigated the influence of hydroalcoholic crude extract of Casearia sylvestris (HCE-CS) and contribution of pro-resolving mediators on mechanical hyperalgesia in a mouse model of chronic post-ischemia pain (CPIP). Methods and resultsMale Swiss mice were subjected to ischemia of the right hind paw (3 h ConclusionThese results reveal significant antihyperalgesic effect of HCE-CS on CPIP, mediated at least in part, by the pathway of resolution of inflammation centred on the axis modulated by ALX/FPR2.

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Aspirin-triggered Lipoxin A4 attenuates mechanical allodynia in association with inhibiting spinal JAK2/STAT3 signaling in neuropathic pain in rats

Cited by 69 publications

References 69 publications

Levetiracetam synergises with common analgesics in producing antinociception in a mouse model of painful diabetic neuropathy

Levetiracetam synergises with common analgesics in producing antinociception in a mouse model of painful diabetic neuropathy

Inhibitory effects of aspirin-triggered resolvin D1 on spinal nociceptive processing in rat pain models

Hydroalcoholic crude extract of Casearia sylvestris Sw. reduces chronic post-ischemic pain by activation of pro-resolving pathways

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