Electroacupuncture improves allodynia and central sensitization via modulation of microglial activation associated P2X4R and inflammation in a rat model of migraine
Recent studies have demonstrated that activated microglia were involved in the pathogenesis of central sensitization characterized by cutaneous allodynia in migraine. Activation of microglia is accompanied by increased expression of its receptors and release of inflammatory mediators. Acupuncture an...
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| Veröffentlicht in: | Molecular pain 2024-01, Vol.20, p.17448069241258113-17448069241258113 |
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| creator | Zhou, Min Pang, Fang Liao, Dongmei Yang, Yunhao Wang, Ying Yang, Zhuxin He, Xinlu Tang, Chenglin |
| description | Recent studies have demonstrated that activated microglia were involved in the pathogenesis of central sensitization characterized by cutaneous allodynia in migraine. Activation of microglia is accompanied by increased expression of its receptors and release of inflammatory mediators. Acupuncture and its developed electroacupuncture (EA) have been recommended as an alternative therapy for migraine and are widely used for relieving migraine-associated pain. However, it remains rare studies that show whether EA exerts anti-migraine effects via inhibiting microglial activation related to a release of microglial receptors and the inflammatory pathway. Therefore, this study aimed to investigate EA' ability to ameliorate central sensitization via modulation of microglial activation, microglial receptor, and inflammatory response using a rat model of migraine induced by repeated epidural chemical stimulation.
In the present study, a rat model of migraine was established by epidural repeated inflammatory soup (IS) stimulation and treated with EA at Fengchi (GB20) and Yanglingquan (GB34) and acupuncture at sham-acupoints. Pain hypersensitivity was further determined by measuring the mechanical withdrawal threshold using the von-Frey filament. The changes in c-Fos and ionized calcium binding adaptor molecule 1 (Ibal-1) labeled microglia in the trigeminal nucleus caudalis (TNC) were examined by immunflurescence to assess the central sensitization and whether accompanied with microglia activation. In addition, the expression of Ibal-1, microglial purinoceptor P2X4, and its associated inflammatory signaling pathway mediators, including interleukin (IL)-1β, NOD-like receptor protein 3 (NLRP3), and Caspase-1 in the TNC were investigated by western blot and real-time polymerase chain reaction analysis.
Allodynia increased of c-Fos, and activated microglia were observed after repeated IS stimulation. EA alleviated the decrease in mechanical withdrawal thresholds, reduced the activation of c-Fos and microglia labeled with Ibal-1, downregulated the level of microglial purinoceptor P2X4, and limited the inflammatory response (NLRP3/Caspase-1/IL-1β signaling pathway) in the TNC of migraine rat model.
Our results indicate that the anti-hyperalgesia effects of EA ameliorate central sensitization in IS-induced migraine by regulating microglial activation related to P2X4R and NLRP3/IL-1β inflammatory pathway. |
| doi_str_mv | 10.1177/17448069241258113 |
| format | Article |
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In the present study, a rat model of migraine was established by epidural repeated inflammatory soup (IS) stimulation and treated with EA at Fengchi (GB20) and Yanglingquan (GB34) and acupuncture at sham-acupoints. Pain hypersensitivity was further determined by measuring the mechanical withdrawal threshold using the von-Frey filament. The changes in c-Fos and ionized calcium binding adaptor molecule 1 (Ibal-1) labeled microglia in the trigeminal nucleus caudalis (TNC) were examined by immunflurescence to assess the central sensitization and whether accompanied with microglia activation. In addition, the expression of Ibal-1, microglial purinoceptor P2X4, and its associated inflammatory signaling pathway mediators, including interleukin (IL)-1β, NOD-like receptor protein 3 (NLRP3), and Caspase-1 in the TNC were investigated by western blot and real-time polymerase chain reaction analysis.
Allodynia increased of c-Fos, and activated microglia were observed after repeated IS stimulation. EA alleviated the decrease in mechanical withdrawal thresholds, reduced the activation of c-Fos and microglia labeled with Ibal-1, downregulated the level of microglial purinoceptor P2X4, and limited the inflammatory response (NLRP3/Caspase-1/IL-1β signaling pathway) in the TNC of migraine rat model.
Our results indicate that the anti-hyperalgesia effects of EA ameliorate central sensitization in IS-induced migraine by regulating microglial activation related to P2X4R and NLRP3/IL-1β inflammatory pathway.</description><identifier>ISSN: 1744-8069</identifier><identifier>EISSN: 1744-8069</identifier><identifier>DOI: 10.1177/17448069241258113</identifier><identifier>PMID: 38744426</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Central Nervous System Sensitization - physiology ; Disease Models, Animal ; Electroacupuncture - methods ; Hyperalgesia - metabolism ; Hyperalgesia - therapy ; Inflammation - metabolism ; Inflammation - pathology ; Inflammation - therapy ; Male ; Microglia - metabolism ; Migraine Disorders - metabolism ; Migraine Disorders - therapy ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; Proto-Oncogene Proteins c-fos - metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Purinergic P2X4 - metabolism</subject><ispartof>Molecular pain, 2024-01, Vol.20, p.17448069241258113-17448069241258113</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c226t-cfa6b25c69e7fa93b1bd383778d211ee4debac56913e12d763f4907c3095b1803</cites><orcidid>0000-0002-9628-9616</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38744426$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Min</creatorcontrib><creatorcontrib>Pang, Fang</creatorcontrib><creatorcontrib>Liao, Dongmei</creatorcontrib><creatorcontrib>Yang, Yunhao</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Yang, Zhuxin</creatorcontrib><creatorcontrib>He, Xinlu</creatorcontrib><creatorcontrib>Tang, Chenglin</creatorcontrib><title>Electroacupuncture improves allodynia and central sensitization via modulation of microglial activation associated P2X4R and inflammation in a rat model of migraine</title><title>Molecular pain</title><addtitle>Mol Pain</addtitle><description>Recent studies have demonstrated that activated microglia were involved in the pathogenesis of central sensitization characterized by cutaneous allodynia in migraine. Activation of microglia is accompanied by increased expression of its receptors and release of inflammatory mediators. Acupuncture and its developed electroacupuncture (EA) have been recommended as an alternative therapy for migraine and are widely used for relieving migraine-associated pain. However, it remains rare studies that show whether EA exerts anti-migraine effects via inhibiting microglial activation related to a release of microglial receptors and the inflammatory pathway. Therefore, this study aimed to investigate EA' ability to ameliorate central sensitization via modulation of microglial activation, microglial receptor, and inflammatory response using a rat model of migraine induced by repeated epidural chemical stimulation.
In the present study, a rat model of migraine was established by epidural repeated inflammatory soup (IS) stimulation and treated with EA at Fengchi (GB20) and Yanglingquan (GB34) and acupuncture at sham-acupoints. Pain hypersensitivity was further determined by measuring the mechanical withdrawal threshold using the von-Frey filament. The changes in c-Fos and ionized calcium binding adaptor molecule 1 (Ibal-1) labeled microglia in the trigeminal nucleus caudalis (TNC) were examined by immunflurescence to assess the central sensitization and whether accompanied with microglia activation. In addition, the expression of Ibal-1, microglial purinoceptor P2X4, and its associated inflammatory signaling pathway mediators, including interleukin (IL)-1β, NOD-like receptor protein 3 (NLRP3), and Caspase-1 in the TNC were investigated by western blot and real-time polymerase chain reaction analysis.
Allodynia increased of c-Fos, and activated microglia were observed after repeated IS stimulation. EA alleviated the decrease in mechanical withdrawal thresholds, reduced the activation of c-Fos and microglia labeled with Ibal-1, downregulated the level of microglial purinoceptor P2X4, and limited the inflammatory response (NLRP3/Caspase-1/IL-1β signaling pathway) in the TNC of migraine rat model.
Our results indicate that the anti-hyperalgesia effects of EA ameliorate central sensitization in IS-induced migraine by regulating microglial activation related to P2X4R and NLRP3/IL-1β inflammatory pathway.</description><subject>Animals</subject><subject>Central Nervous System Sensitization - physiology</subject><subject>Disease Models, Animal</subject><subject>Electroacupuncture - methods</subject><subject>Hyperalgesia - metabolism</subject><subject>Hyperalgesia - therapy</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Inflammation - therapy</subject><subject>Male</subject><subject>Microglia - metabolism</subject><subject>Migraine Disorders - metabolism</subject><subject>Migraine Disorders - therapy</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>Proto-Oncogene Proteins c-fos - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Purinergic P2X4 - metabolism</subject><issn>1744-8069</issn><issn>1744-8069</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNplkd9KHTEQxoNU1FofwJuSy96cNn92k91LEW0LQkUs9G6ZTWYlJZsck-wB-zx90OZ0rQi9msx8v_lg8hFyztlHzrX-xHXTdEz1ouGi7TiXB-RkP9vsh29evY_J25x_MiY1U_yIHMuuKo1QJ-T3lUdTUgSzbJdgypKQunmb4g4zBe-jfQoOKARLDYaSwNOMIbvifkFxMdBdVedoF7-2caKzMyk-eFdRMMXtVgFyjsZBQUtvxY_m7q-lC5OHeV4JVyGaoOzt0K9ODwlcwHfkcAKf8ey5npLv11f3l182N98-f728uNkYIVTZmAnUKFqjetQT9HLko5Wd1LqzgnPExuIIplU9l8iF1UpOTc-0kaxvR94xeUo-rL71_scFcxlmlw16DwHjkgfJ2rZp6zeqivIVrbfmnHAatsnNkJ4GzoZ9OMN_4dSd98_2yzijfdn4l4b8A7GqjbI</recordid><startdate>202401</startdate><enddate>202401</enddate><creator>Zhou, Min</creator><creator>Pang, Fang</creator><creator>Liao, Dongmei</creator><creator>Yang, Yunhao</creator><creator>Wang, Ying</creator><creator>Yang, Zhuxin</creator><creator>He, Xinlu</creator><creator>Tang, Chenglin</creator><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><orcidid>https://orcid.org/0000-0002-9628-9616</orcidid></search><sort><creationdate>202401</creationdate><title>Electroacupuncture improves allodynia and central sensitization via modulation of microglial activation associated P2X4R and inflammation in a rat model of migraine</title><author>Zhou, Min ; Pang, Fang ; Liao, Dongmei ; Yang, Yunhao ; Wang, Ying ; Yang, Zhuxin ; He, Xinlu ; Tang, Chenglin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c226t-cfa6b25c69e7fa93b1bd383778d211ee4debac56913e12d763f4907c3095b1803</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Central Nervous System Sensitization - physiology</topic><topic>Disease Models, Animal</topic><topic>Electroacupuncture - methods</topic><topic>Hyperalgesia - metabolism</topic><topic>Hyperalgesia - therapy</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Inflammation - therapy</topic><topic>Male</topic><topic>Microglia - metabolism</topic><topic>Migraine Disorders - metabolism</topic><topic>Migraine Disorders - therapy</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>Proto-Oncogene Proteins c-fos - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Purinergic P2X4 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Min</creatorcontrib><creatorcontrib>Pang, Fang</creatorcontrib><creatorcontrib>Liao, Dongmei</creatorcontrib><creatorcontrib>Yang, Yunhao</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Yang, Zhuxin</creatorcontrib><creatorcontrib>He, Xinlu</creatorcontrib><creatorcontrib>Tang, Chenglin</creatorcontrib><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><jtitle>Molecular pain</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Min</au><au>Pang, Fang</au><au>Liao, Dongmei</au><au>Yang, Yunhao</au><au>Wang, Ying</au><au>Yang, Zhuxin</au><au>He, Xinlu</au><au>Tang, Chenglin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Electroacupuncture improves allodynia and central sensitization via modulation of microglial activation associated P2X4R and inflammation in a rat model of migraine</atitle><jtitle>Molecular pain</jtitle><addtitle>Mol Pain</addtitle><date>2024-01</date><risdate>2024</risdate><volume>20</volume><spage>17448069241258113</spage><epage>17448069241258113</epage><pages>17448069241258113-17448069241258113</pages><issn>1744-8069</issn><eissn>1744-8069</eissn><abstract>Recent studies have demonstrated that activated microglia were involved in the pathogenesis of central sensitization characterized by cutaneous allodynia in migraine. Activation of microglia is accompanied by increased expression of its receptors and release of inflammatory mediators. Acupuncture and its developed electroacupuncture (EA) have been recommended as an alternative therapy for migraine and are widely used for relieving migraine-associated pain. However, it remains rare studies that show whether EA exerts anti-migraine effects via inhibiting microglial activation related to a release of microglial receptors and the inflammatory pathway. Therefore, this study aimed to investigate EA' ability to ameliorate central sensitization via modulation of microglial activation, microglial receptor, and inflammatory response using a rat model of migraine induced by repeated epidural chemical stimulation.
In the present study, a rat model of migraine was established by epidural repeated inflammatory soup (IS) stimulation and treated with EA at Fengchi (GB20) and Yanglingquan (GB34) and acupuncture at sham-acupoints. Pain hypersensitivity was further determined by measuring the mechanical withdrawal threshold using the von-Frey filament. The changes in c-Fos and ionized calcium binding adaptor molecule 1 (Ibal-1) labeled microglia in the trigeminal nucleus caudalis (TNC) were examined by immunflurescence to assess the central sensitization and whether accompanied with microglia activation. In addition, the expression of Ibal-1, microglial purinoceptor P2X4, and its associated inflammatory signaling pathway mediators, including interleukin (IL)-1β, NOD-like receptor protein 3 (NLRP3), and Caspase-1 in the TNC were investigated by western blot and real-time polymerase chain reaction analysis.
Allodynia increased of c-Fos, and activated microglia were observed after repeated IS stimulation. EA alleviated the decrease in mechanical withdrawal thresholds, reduced the activation of c-Fos and microglia labeled with Ibal-1, downregulated the level of microglial purinoceptor P2X4, and limited the inflammatory response (NLRP3/Caspase-1/IL-1β signaling pathway) in the TNC of migraine rat model.
Our results indicate that the anti-hyperalgesia effects of EA ameliorate central sensitization in IS-induced migraine by regulating microglial activation related to P2X4R and NLRP3/IL-1β inflammatory pathway.</abstract><cop>United States</cop><pmid>38744426</pmid><doi>10.1177/17448069241258113</doi><orcidid>https://orcid.org/0000-0002-9628-9616</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Central Nervous System Sensitization - physiology Disease Models, Animal Electroacupuncture - methods Hyperalgesia - metabolism Hyperalgesia - therapy Inflammation - metabolism Inflammation - pathology Inflammation - therapy Male Microglia - metabolism Migraine Disorders - metabolism Migraine Disorders - therapy NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Proto-Oncogene Proteins c-fos - metabolism Rats Rats, Sprague-Dawley Receptors, Purinergic P2X4 - metabolism |
| title | Electroacupuncture improves allodynia and central sensitization via modulation of microglial activation associated P2X4R and inflammation in a rat model of migraine |
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