2023
DOI: 10.3390/cells12091275
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Therapeutic Effects of Combined Treatment with the AEA Hydrolysis Inhibitor PF04457845 and the Substrate Selective COX-2 Inhibitor LM4131 in the Mouse Model of Neuropathic Pain

Abstract: Chronic neuropathic pain resulting from peripheral nerve damage is a significant clinical problem, which makes it imperative to develop the mechanism-based therapeutic approaches. Enhancement of endogenous cannabinoids by blocking their hydrolysis has been shown to reduce inflammation and neuronal damage in a number of neurological disorders and neurodegenerative diseases. However, recent studies suggest that inhibition of their hydrolysis can shift endocannabinoids 2-arachidonoyl glycerol (2-AG) and anandamid… Show more

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Cited by 3 publications
(1 citation statement)
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“…Nonetheless, in both experimental paradigms, the FAAH inhibitor proved to be able to reduce the IoN-CCI-induced upregulation of the pain neuropeptide CGRP and proinflammatory cytokines TNF-alpha and IL-1beta and to increase the anti-inflammatory cytokine IL-10 in trigeminal-related areas. The present findings are consistent with previous studies in which FAAH inhibitors were able to alter the gene expression of pain and inflammatory mediators [33][34][35][36][37][38]. However, based on the discrepancies observed in these two different experimental settings, it appears that changes in gene expression of the mediators evaluated in this study are not directly associated with mechanical pain, thus suggesting that other signalling pathways and mediators are involved.…”
Section: Discussionsupporting
confidence: 92%
“…Nonetheless, in both experimental paradigms, the FAAH inhibitor proved to be able to reduce the IoN-CCI-induced upregulation of the pain neuropeptide CGRP and proinflammatory cytokines TNF-alpha and IL-1beta and to increase the anti-inflammatory cytokine IL-10 in trigeminal-related areas. The present findings are consistent with previous studies in which FAAH inhibitors were able to alter the gene expression of pain and inflammatory mediators [33][34][35][36][37][38]. However, based on the discrepancies observed in these two different experimental settings, it appears that changes in gene expression of the mediators evaluated in this study are not directly associated with mechanical pain, thus suggesting that other signalling pathways and mediators are involved.…”
Section: Discussionsupporting
confidence: 92%