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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
Citation
Molecular Pain,  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

 

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, -
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.relation.ispartofMolecular Pain-
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.identifier.hkuros281046-

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