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Article: Propofol produces preventive analgesia via GluN2B-containing NMDA Receptor/ERK1/2 Signaling Pathway in the rat model of Inflammatory Pain

TitlePropofol produces preventive analgesia via GluN2B-containing NMDA Receptor/ERK1/2 Signaling Pathway in the rat model of Inflammatory Pain
Authors
Issue Date2017
PublisherSAGE Publications (UK and US): Open Access Titles. The Journal's web site is located at http://mpx.sagepub.com/home/
Citation
Molecular Pain, 2017, v. 13, p. 1-13 How to Cite?
AbstractCompared to other anesthetics, propofol has showed superior analgesic effect used during surgical procedures on acute post-surgical pain. Whether propofol has preventive analgesic property remain debated. The present study investigated the antinociceptive effect of propofol and underlying molecular and cellular mechanisms via pre-emptive administration in a formalin-induced inflammatory pain model in rats. Male adult Sprague-Dawley rats were randomly allocated into 4 groups: naïve (Group Naïve), formalin injection only (Group Formalin), and formalin injection at 30 min (Group P-30min) or 2 h (Group P-2h) after intravenous infusion of propofol (0.6 mg kg-1 min-1) for 1 h. Nociceptive responses were evaluated by composite pain score-weighted scores. Protein expression of phosphorylated- or pan-GluN2B, ERK1/2, p38 MAPK and JNK in the spinal dorsal horn was assessed by Western blot. Alteration of intracellular Ca2+ concentration induced by NMDA receptor agonists with or without pre-treatment of propofol was measured using fluorometry in SH-SY5Y cells. Neuronal activation was assessed by immunofluorescence. Pre-emptive propofol reduced pain with a delayed response to formalin and a reduction in hypersensitivity that lasted at least for 2 h. The formalin-induced activation of spinal GluN2B and ERK1/2 but not p38 or JNK were also diminished by propofol treatment. Preconditioning treatment with 3 µM and 10 µM of propofol inhibited Ca2+ influx mediated through NMDA receptors in SH-SY5Y cells. Propofol also reduced the neuronal expression of c-Fos and p-ERK induced by formalin. These findings indicate that pre-emptive administration of propofol produces preventive analgesic effects on inflammatory pain through regulating neuronal GluN2B-containing NMDA receptor and ERK1/2 pathway in the spinal dorsal horn.
Persistent Identifierhttp://hdl.handle.net/10722/248300
ISSN
2015 Impact Factor: 3.07
2015 SCImago Journal Rankings: 1.704
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorQiu, Q-
dc.contributor.authorSun, LT-
dc.contributor.authorGU, P-
dc.contributor.authorShiu, HC-
dc.contributor.authorWang, XMA-
dc.contributor.authorLo, ACY-
dc.contributor.authorWong, K-
dc.contributor.authorLi, Q-
dc.contributor.authorWong, SCS-
dc.contributor.authorCheung, CW-
dc.date.accessioned2017-10-18T08:41:03Z-
dc.date.available2017-10-18T08:41:03Z-
dc.date.issued2017-
dc.identifier.citationMolecular Pain, 2017, v. 13, p. 1-13-
dc.identifier.issn1744-8069-
dc.identifier.urihttp://hdl.handle.net/10722/248300-
dc.description.abstractCompared to other anesthetics, propofol has showed superior analgesic effect used during surgical procedures on acute post-surgical pain. Whether propofol has preventive analgesic property remain debated. The present study investigated the antinociceptive effect of propofol and underlying molecular and cellular mechanisms via pre-emptive administration in a formalin-induced inflammatory pain model in rats. Male adult Sprague-Dawley rats were randomly allocated into 4 groups: naïve (Group Naïve), formalin injection only (Group Formalin), and formalin injection at 30 min (Group P-30min) or 2 h (Group P-2h) after intravenous infusion of propofol (0.6 mg kg-1 min-1) for 1 h. Nociceptive responses were evaluated by composite pain score-weighted scores. Protein expression of phosphorylated- or pan-GluN2B, ERK1/2, p38 MAPK and JNK in the spinal dorsal horn was assessed by Western blot. Alteration of intracellular Ca2+ concentration induced by NMDA receptor agonists with or without pre-treatment of propofol was measured using fluorometry in SH-SY5Y cells. Neuronal activation was assessed by immunofluorescence. Pre-emptive propofol reduced pain with a delayed response to formalin and a reduction in hypersensitivity that lasted at least for 2 h. The formalin-induced activation of spinal GluN2B and ERK1/2 but not p38 or JNK were also diminished by propofol treatment. Preconditioning treatment with 3 µM and 10 µM of propofol inhibited Ca2+ influx mediated through NMDA receptors in SH-SY5Y cells. Propofol also reduced the neuronal expression of c-Fos and p-ERK induced by formalin. These findings indicate that pre-emptive administration of propofol produces preventive analgesic effects on inflammatory pain through regulating neuronal GluN2B-containing NMDA receptor and ERK1/2 pathway in the spinal dorsal horn.-
dc.languageeng-
dc.publisherSAGE Publications (UK and US): Open Access Titles. The Journal's web site is located at http://mpx.sagepub.com/home/-
dc.relation.ispartofMolecular Pain-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titlePropofol produces preventive analgesia via GluN2B-containing NMDA Receptor/ERK1/2 Signaling Pathway in the rat model of Inflammatory Pain-
dc.typeArticle-
dc.identifier.emailSun, LT: ltsun@hku.hk-
dc.identifier.emailShiu, HC: hoicshiu@hku.hk-
dc.identifier.emailWang, XMA: xmwang1@hku.hk-
dc.identifier.emailLo, ACY: amylo@hku.hk-
dc.identifier.emailWong, K: wongeric@hku.hk-
dc.identifier.emailWong, SCS: wongstan@hku.hk-
dc.identifier.emailCheung, CW: cheucw@hku.hk-
dc.identifier.authorityLo, ACY=rp00425-
dc.identifier.authorityWong, SCS=rp01789-
dc.identifier.authorityCheung, CW=rp00244-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1177/1744806917737462-
dc.identifier.pmcidPMC5644366-
dc.identifier.hkuros281046-
dc.identifier.volume13-
dc.identifier.spage1-
dc.identifier.epage13-
dc.publisher.placeUnited Kingdom-

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