Non-opioid Analgesics and the Endocannabinoid System
Non-steroidal anti-inflammatory drugs produce antinociceptive effects mainly through peripheral cyclooxygenase inhibition. In opposition to the classical non-steroidal anti-inflammatory drugs, paracetamol and dipyrone exert weak anti-inflammatory activity, their antinociceptive effects appearing to...
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Published in | Balkan medical journal Vol. 37; no. 6; pp. 309 - 315 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Galenos Yayinevi Tic. Ltd
01.11.2020
Trakya Üniversitesi Galenos Publishing Galenos Publishing House |
Subjects | |
Online Access | Get full text |
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Abstract | Non-steroidal anti-inflammatory drugs produce antinociceptive effects mainly through peripheral cyclooxygenase inhibition. In opposition to the classical non-steroidal anti-inflammatory drugs, paracetamol and dipyrone exert weak anti-inflammatory activity, 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. Keywords: Dipyrone, endocannabinoids, NSAIDs, paracetamol |
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AbstractList | Non-steroidal anti-inflammatory drugs produce antinociceptive
effects mainly through peripheral cyclooxygenase inhibition.
In opposition to the classical non-steroidal anti-inflammatory
drugs, paracetamol and dipyrone exert weak anti-inflammatory
activity, 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. Non-steroidal anti-inflammatory drugs produce antinociceptive effects mainly through peripheral cyclooxygenase inhibition. In opposition to the classical non-steroidal anti-inflammatory drugs, paracetamol and dipyrone exert weak anti-inflammatory activity, 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. Keywords: Dipyrone, endocannabinoids, NSAIDs, paracetamol Non-steroidal anti-inflammatory drugs produce antinociceptive effects mainly through peripheral cyclooxygenase inhibition. In opposition to the classical non-steroidal anti-inflammatory drugs, paracetamol and dipyrone exert weak anti-inflammatory activity, 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. |
Audience | Academic |
Author | Ulugöl, Ahmet Topuz, Ruhan Deniz Karadağ, Çetin Hakan Gündüz, Özgur |
AuthorAffiliation | Dahili Tıp Bilimleri Bölümü, Tıbbi Farmakoloji Anabilim Dalı |
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SubjectTerms | Acetaminophen dipyrone Endocannabinoids Health aspects Invited Review Nonsteroidal anti-inflammatory agents nsaids paracetamol Physiological aspects Tıp |
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