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Journals / Balkan Medical Journal / 2020 / Cilt: 37 - Sayı: 6

Non-opioid Analgesics and the Endocannabinoid System

Ahmet ULUGÖL
Ruhan Deniz TOPUZ
Çetin Hakan KARADAĞ
Özgür GÜNDÜZ
Pages
309–315
Publication Date
2022-10-11
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Non-opioid analgesics and their metabolites may activate cannabinoid receptors, as well as elevate endocannabinoid levels through different mechanisms: reduction of endocannabinoid degradation via fatty acid amide hydrolase and/or cyclooxygenase-2 inhibition, mobilization of arachidonic acid for the biosynthesis of endocannabinoids due to cyclooxygenase inhibition, inhibition of endocannabinoid cellular uptake directly or through the inhibition of nitric oxide synthase production, and induction of endocannabinoid release.

📌 3 Key Takeaways

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Objective & Hypothesis:Non-steroidalanti-inflammatorydrugsproduceantinociceptiveeffectsmainlythroughperipheralcyclooxygenaseinhibition.Inoppositiontotheclassicalnon-steroidalanti-inflammatorydrugs,paracetamolanddipyroneexertweakanti-inflammatoryactivity, their antinociceptive effects appearing to be mostly due to mechanisms other than peripheral cyclooxygenase inhibition.
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Key Findings & Data:In this review, we classify classical non-steroidal anti-inflammatory drugs, paracetamol and dipyrone as “non-opioid analgesics” and discuss the mechanisms mediating participation of the endocannabinoid system in their antinociceptive effects.
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Conclusion & Impact:Non-opioid analgesics and their metabolites may activate cannabinoid receptors, as well as elevate endocannabinoid levels through different mechanisms: reduction of endocannabinoid degradation via fatty acid amide hydrolase and/or cyclooxygenase-2 inhibition, mobilization of arachidonic acid for the biosynthesis of endocannabinoids due to cyclooxygenase inhibition, inhibition of endocannabinoid cellular uptake directly or through the inhibition of nitric oxide synthase production, and induction of endocannabinoid release.
🔬Design:Review & Systematic Survey
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Non-steroidalanti-inflammatorydrugsproduceantinociceptiveeffectsmainlythroughperipheralcyclooxygenaseinhibition.Inoppositiontotheclassicalnon-steroidalanti-inflammatorydrugs,paracetamolanddipyroneexertweakanti-inflammatoryactivity, their antinociceptive effects appearing to be mostly due to mechanisms other than peripheral cyclooxygenase inhibition. In this review, we classify classical non-steroidal anti-inflammatory drugs, paracetamol and dipyrone as “non-opioid analgesics” and discuss the mechanisms mediating participation of the endocannabinoid system in their antinociceptive effects. Non-opioid analgesics and their metabolites may activate cannabinoid receptors, as well as elevate endocannabinoid levels through different mechanisms: reduction of endocannabinoid degradation via fatty acid amide hydrolase and/or cyclooxygenase-2 inhibition, mobilization of arachidonic acid for the biosynthesis of endocannabinoids due to cyclooxygenase inhibition, inhibition of endocannabinoid cellular uptake directly or through the inhibition of nitric oxide synthase production, and induction of endocannabinoid release.

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Cite This Article

ULUGÖL, A., TOPUZ, R. D., KARADAĞ, Ç. H., GÜNDÜZ, Ö. (2022). Non-opioid Analgesics and the Endocannabinoid System. Balkan Medical Journal, Cilt: 37 - Sayı: 6, 309–315. https://ajindex.com/articles/460856

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