Inhibition of ROS-induced p38MAPK and ERK activation in microglia by acupuncture relieves neuropathic pain after spinal cord injury in rats
Acupuncture (AP) is currently used worldwide to relieve pain. However, little is known about its mechanisms of action. We found that after spinal cord injury (SCI), AP inhibited the production of superoxide anion (O2), which acted as a modulator for microglial activation, and the analgesic effect of...
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description | Acupuncture (AP) is currently used worldwide to relieve pain. However, little is known about its mechanisms of action. We found that after spinal cord injury (SCI), AP inhibited the production of superoxide anion (O2), which acted as a modulator for microglial activation, and the analgesic effect of AP was attributed to its anti-microglial activating action. Direct injection of a ROS scavenger inhibited SCI-induced NP. After contusion injury which induces the below-level neuropathic pain (NP), Shuigou and Yanglingquan acupoints were applied. AP relieved mechanical allodynia and thermal hyperalgesia, while vehicle and simulated AP did not. AP also decreased the proportion of activated microglia, and inhibited both p38MAPK and ERK activation in microglia at the L4–5. Also, the level of prostaglandin E2 (PGE2), which is produced via ERK signaling and mediates the below-level pain through PGE2 receptor, was reduced by AP. Injection of p38MAPK or ERK inhibitors attenuated NP and decreased PGE2 production. Furthermore, ROS produced after injury‐induced p38MAPK and ERK activation in microglia, and mediated mechanical allodynia and thermal hyperalgesia, which were inhibited by AP or a ROS scavenger. AP also inhibited the expression of inflammatory mediators. Therefore, our results suggest that the analgesic effect of AP may be partly mediated by inhibiting ROS-induced microglial activation and inflammatory responses after SCI and provide the possibility that AP can be used effectively as a non-pharmacological intervention for SCI-induced chronic NP in patients.
► Acupuncture (AP) relieved neuropathic pain developed after spinal cord injury. ► AP inhibited ROS‐induced p38MAPK and ERK activation in microglia after SCI. ► AP also inhibited ERK-dependent PGE2 production after SCI. ► AP can be used as non-pharmacological intervention for SCI-induced neuropathic pain. |
doi_str_mv | 10.1016/j.expneurol.2012.05.014 |
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► Acupuncture (AP) relieved neuropathic pain developed after spinal cord injury. ► AP inhibited ROS‐induced p38MAPK and ERK activation in microglia after SCI. ► AP also inhibited ERK-dependent PGE2 production after SCI. ► AP can be used as non-pharmacological intervention for SCI-induced neuropathic pain.</description><identifier>ISSN: 0014-4886</identifier><identifier>EISSN: 1090-2430</identifier><identifier>DOI: 10.1016/j.expneurol.2012.05.014</identifier><identifier>PMID: 22634758</identifier><identifier>CODEN: EXNEAC</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>Acupuncture ; Acupuncture Therapy - methods ; Analgesics ; Animals ; Biological and medical sciences ; Central neuropathic pain ; Chronic Disease ; Disease Models, Animal ; Enzyme Activation - physiology ; Extracellular signal-regulated kinase ; Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Inflammation ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Male ; MAPK kinase ; Medical sciences ; Microglia ; Microglia - enzymology ; Microglia - pathology ; Neuralgia - enzymology ; Neuralgia - etiology ; Neuralgia - therapy ; Neurology ; Neuromodulation ; Neuropathy ; p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases - metabolism ; Pain Measurement - methods ; Pain perception ; Prostaglandin E2 ; Rats ; Rats, Sprague-Dawley ; Reactive oxygen species ; Reactive Oxygen Species - administration & dosage ; Reactive Oxygen Species - antagonists & inhibitors ; Spinal Cord Injuries - complications ; Spinal Cord Injuries - enzymology ; Spinal Cord Injuries - therapy ; Spinal cord injury ; superoxide anions ; Traumas. Diseases due to physical agents</subject><ispartof>Experimental neurology, 2012-08, Vol.236 (2), p.268-282</ispartof><rights>2012</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2012. Published by Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c460t-fd4fca318a6f4a77a2dd27f359535ebaffd5d9a31836d4fa9238598ed6f0b88f3</citedby><cites>FETCH-LOGICAL-c460t-fd4fca318a6f4a77a2dd27f359535ebaffd5d9a31836d4fa9238598ed6f0b88f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.expneurol.2012.05.014$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26204698$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22634758$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Choi, Doo C.</creatorcontrib><creatorcontrib>Lee, Jee Y.</creatorcontrib><creatorcontrib>Lim, Eun J.</creatorcontrib><creatorcontrib>Baik, Hyung H.</creatorcontrib><creatorcontrib>Oh, Tae H.</creatorcontrib><creatorcontrib>Yune, Tae Y.</creatorcontrib><title>Inhibition of ROS-induced p38MAPK and ERK activation in microglia by acupuncture relieves neuropathic pain after spinal cord injury in rats</title><title>Experimental neurology</title><addtitle>Exp Neurol</addtitle><description>Acupuncture (AP) is currently used worldwide to relieve pain. However, little is known about its mechanisms of action. We found that after spinal cord injury (SCI), AP inhibited the production of superoxide anion (O2), which acted as a modulator for microglial activation, and the analgesic effect of AP was attributed to its anti-microglial activating action. Direct injection of a ROS scavenger inhibited SCI-induced NP. After contusion injury which induces the below-level neuropathic pain (NP), Shuigou and Yanglingquan acupoints were applied. AP relieved mechanical allodynia and thermal hyperalgesia, while vehicle and simulated AP did not. AP also decreased the proportion of activated microglia, and inhibited both p38MAPK and ERK activation in microglia at the L4–5. Also, the level of prostaglandin E2 (PGE2), which is produced via ERK signaling and mediates the below-level pain through PGE2 receptor, was reduced by AP. Injection of p38MAPK or ERK inhibitors attenuated NP and decreased PGE2 production. Furthermore, ROS produced after injury‐induced p38MAPK and ERK activation in microglia, and mediated mechanical allodynia and thermal hyperalgesia, which were inhibited by AP or a ROS scavenger. AP also inhibited the expression of inflammatory mediators. Therefore, our results suggest that the analgesic effect of AP may be partly mediated by inhibiting ROS-induced microglial activation and inflammatory responses after SCI and provide the possibility that AP can be used effectively as a non-pharmacological intervention for SCI-induced chronic NP in patients.
► Acupuncture (AP) relieved neuropathic pain developed after spinal cord injury. ► AP inhibited ROS‐induced p38MAPK and ERK activation in microglia after SCI. ► AP also inhibited ERK-dependent PGE2 production after SCI. ► AP can be used as non-pharmacological intervention for SCI-induced neuropathic pain.</description><subject>Acupuncture</subject><subject>Acupuncture Therapy - methods</subject><subject>Analgesics</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Central neuropathic pain</subject><subject>Chronic Disease</subject><subject>Disease Models, Animal</subject><subject>Enzyme Activation - physiology</subject><subject>Extracellular signal-regulated kinase</subject><subject>Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Inflammation</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Male</subject><subject>MAPK kinase</subject><subject>Medical sciences</subject><subject>Microglia</subject><subject>Microglia - enzymology</subject><subject>Microglia - pathology</subject><subject>Neuralgia - enzymology</subject><subject>Neuralgia - etiology</subject><subject>Neuralgia - therapy</subject><subject>Neurology</subject><subject>Neuromodulation</subject><subject>Neuropathy</subject><subject>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Pain Measurement - methods</subject><subject>Pain perception</subject><subject>Prostaglandin E2</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - administration & dosage</subject><subject>Reactive Oxygen Species - antagonists & inhibitors</subject><subject>Spinal Cord Injuries - complications</subject><subject>Spinal Cord Injuries - enzymology</subject><subject>Spinal Cord Injuries - therapy</subject><subject>Spinal cord injury</subject><subject>superoxide anions</subject><subject>Traumas. Diseases due to physical agents</subject><issn>0014-4886</issn><issn>1090-2430</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhS0EokPhFcAbJDYJ_ovjLEdVgYqiogJry2NfU48yTrCTEfMMvDROZyhLWF3p-jvHV-cg9IqSmhIq325r-DlGmNPQ14xQVpOmJlQ8QitKOlIxwcljtCJlVQml5Bl6lvOWENIJ1j5FZ4xJLtpGrdCvq3gXNmEKQ8SDx7c3X6oQ3WzB4ZGrT-vPH7GJDl_elmmnsDf3ZIh4F2wavvfB4M2hPM3jHO00J8AJ-gB7yPj-vNFMd8Hi0RSJ8RMknMcQTY_tkFzx2c7psNglM-Xn6Ik3fYYXp3mOvr27_Hrxobq-eX91sb6urJBkqrwT3hpOlZFemLY1zDnWet50DW9gY7x3jesWgMuCmo5x1XQKnPRko5Tn5-jN0XdMw48Z8qR3IVvoexNhmLOmhCtJW0Lpf6Al6oYIRQraHtGSS84JvB5T2Jl0KJBeStNb_VCaXkrTpNGloaJ8efpk3uzAPej-tFSA1yfAZGt6n0y0If_lJCNCdgu3PnJQ0tsHSDrbALGUGRLYSbsh_POY3z4cu4k</recordid><startdate>20120801</startdate><enddate>20120801</enddate><creator>Choi, Doo C.</creator><creator>Lee, Jee Y.</creator><creator>Lim, Eun J.</creator><creator>Baik, Hyung H.</creator><creator>Oh, Tae H.</creator><creator>Yune, Tae Y.</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7TK</scope></search><sort><creationdate>20120801</creationdate><title>Inhibition of ROS-induced p38MAPK and ERK activation in microglia by acupuncture relieves neuropathic pain after spinal cord injury in rats</title><author>Choi, Doo C. ; Lee, Jee Y. ; Lim, Eun J. ; Baik, Hyung H. ; Oh, Tae H. ; Yune, Tae Y.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c460t-fd4fca318a6f4a77a2dd27f359535ebaffd5d9a31836d4fa9238598ed6f0b88f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acupuncture</topic><topic>Acupuncture Therapy - methods</topic><topic>Analgesics</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Central neuropathic pain</topic><topic>Chronic Disease</topic><topic>Disease Models, Animal</topic><topic>Enzyme Activation - physiology</topic><topic>Extracellular signal-regulated kinase</topic><topic>Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Inflammation</topic><topic>Injuries of the nervous system and the skull. Diseases due to physical agents</topic><topic>Male</topic><topic>MAPK kinase</topic><topic>Medical sciences</topic><topic>Microglia</topic><topic>Microglia - enzymology</topic><topic>Microglia - pathology</topic><topic>Neuralgia - enzymology</topic><topic>Neuralgia - etiology</topic><topic>Neuralgia - therapy</topic><topic>Neurology</topic><topic>Neuromodulation</topic><topic>Neuropathy</topic><topic>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Pain Measurement - methods</topic><topic>Pain perception</topic><topic>Prostaglandin E2</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - administration & dosage</topic><topic>Reactive Oxygen Species - antagonists & inhibitors</topic><topic>Spinal Cord Injuries - complications</topic><topic>Spinal Cord Injuries - enzymology</topic><topic>Spinal Cord Injuries - therapy</topic><topic>Spinal cord injury</topic><topic>superoxide anions</topic><topic>Traumas. Diseases due to physical agents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Choi, Doo C.</creatorcontrib><creatorcontrib>Lee, Jee Y.</creatorcontrib><creatorcontrib>Lim, Eun J.</creatorcontrib><creatorcontrib>Baik, Hyung H.</creatorcontrib><creatorcontrib>Oh, Tae H.</creatorcontrib><creatorcontrib>Yune, Tae Y.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Experimental neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Choi, Doo C.</au><au>Lee, Jee Y.</au><au>Lim, Eun J.</au><au>Baik, Hyung H.</au><au>Oh, Tae H.</au><au>Yune, Tae Y.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of ROS-induced p38MAPK and ERK activation in microglia by acupuncture relieves neuropathic pain after spinal cord injury in rats</atitle><jtitle>Experimental neurology</jtitle><addtitle>Exp Neurol</addtitle><date>2012-08-01</date><risdate>2012</risdate><volume>236</volume><issue>2</issue><spage>268</spage><epage>282</epage><pages>268-282</pages><issn>0014-4886</issn><eissn>1090-2430</eissn><coden>EXNEAC</coden><abstract>Acupuncture (AP) is currently used worldwide to relieve pain. However, little is known about its mechanisms of action. We found that after spinal cord injury (SCI), AP inhibited the production of superoxide anion (O2), which acted as a modulator for microglial activation, and the analgesic effect of AP was attributed to its anti-microglial activating action. Direct injection of a ROS scavenger inhibited SCI-induced NP. After contusion injury which induces the below-level neuropathic pain (NP), Shuigou and Yanglingquan acupoints were applied. AP relieved mechanical allodynia and thermal hyperalgesia, while vehicle and simulated AP did not. AP also decreased the proportion of activated microglia, and inhibited both p38MAPK and ERK activation in microglia at the L4–5. Also, the level of prostaglandin E2 (PGE2), which is produced via ERK signaling and mediates the below-level pain through PGE2 receptor, was reduced by AP. Injection of p38MAPK or ERK inhibitors attenuated NP and decreased PGE2 production. Furthermore, ROS produced after injury‐induced p38MAPK and ERK activation in microglia, and mediated mechanical allodynia and thermal hyperalgesia, which were inhibited by AP or a ROS scavenger. AP also inhibited the expression of inflammatory mediators. Therefore, our results suggest that the analgesic effect of AP may be partly mediated by inhibiting ROS-induced microglial activation and inflammatory responses after SCI and provide the possibility that AP can be used effectively as a non-pharmacological intervention for SCI-induced chronic NP in patients.
► Acupuncture (AP) relieved neuropathic pain developed after spinal cord injury. ► AP inhibited ROS‐induced p38MAPK and ERK activation in microglia after SCI. ► AP also inhibited ERK-dependent PGE2 production after SCI. ► AP can be used as non-pharmacological intervention for SCI-induced neuropathic pain.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>22634758</pmid><doi>10.1016/j.expneurol.2012.05.014</doi><tpages>15</tpages></addata></record> |
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subjects | Acupuncture Acupuncture Therapy - methods Analgesics Animals Biological and medical sciences Central neuropathic pain Chronic Disease Disease Models, Animal Enzyme Activation - physiology Extracellular signal-regulated kinase Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors Extracellular Signal-Regulated MAP Kinases - metabolism Inflammation Injuries of the nervous system and the skull. Diseases due to physical agents Male MAPK kinase Medical sciences Microglia Microglia - enzymology Microglia - pathology Neuralgia - enzymology Neuralgia - etiology Neuralgia - therapy Neurology Neuromodulation Neuropathy p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors p38 Mitogen-Activated Protein Kinases - metabolism Pain Measurement - methods Pain perception Prostaglandin E2 Rats Rats, Sprague-Dawley Reactive oxygen species Reactive Oxygen Species - administration & dosage Reactive Oxygen Species - antagonists & inhibitors Spinal Cord Injuries - complications Spinal Cord Injuries - enzymology Spinal Cord Injuries - therapy Spinal cord injury superoxide anions Traumas. Diseases due to physical agents |
title | Inhibition of ROS-induced p38MAPK and ERK activation in microglia by acupuncture relieves neuropathic pain after spinal cord injury in rats |
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