CDDO regulates central and peripheral sensitization to attenuate post‐herpetic neuralgia by targeting TRPV1/PKC‐δ/p‐Akt signals
Postherpetic neuralgia (PHN) is a notorious neuropathic pain featuring persistent profound mechanical hyperalgesia with significant negative impact on patients' life quality. CDDO can regulate inflammatory response and programmed cell death. Its derivative also protects neurons from damages by...
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description | Postherpetic neuralgia (PHN) is a notorious neuropathic pain featuring persistent profound mechanical hyperalgesia with significant negative impact on patients' life quality. CDDO can regulate inflammatory response and programmed cell death. Its derivative also protects neurons from damages by modulating microglia activities. As a consequence of central and peripheral sensitization, applying neural blocks may benefit to minimize the risk of PHN. This study aimed to explore whether CDDO could generate analgesic action in a PHN‐rats' model. The behavioural test was determined by calibrated forceps testing. The number of apoptotic neurons and degree of glial cell reaction were assessed by immunofluorescence assay. Activation of PKC‐δ and the phosphorylation of Akt were measured by western blots. CDDO improved PHN by decreasing TRPV1‐positive nociceptive neurons, the apoptotic neurons, and reversed glial cell reaction in adult rats. It also suppressed the enhanced PKC‐δ and p‐Akt signalling in the sciatic nerve, dorsal root ganglia (DRG) and spinal dorsal horn. Our research is the promising report demonstrating the analgesic and neuroprotective action of CDDO in a PHN‐rat's model by regulating central and peripheral sensitization targeting TRPV1, PKC‐δ and p‐Akt. It also is the first study to elucidate the role of oligodendrocyte in PHN. |
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CDDO can regulate inflammatory response and programmed cell death. Its derivative also protects neurons from damages by modulating microglia activities. As a consequence of central and peripheral sensitization, applying neural blocks may benefit to minimize the risk of PHN. This study aimed to explore whether CDDO could generate analgesic action in a PHN‐rats' model. The behavioural test was determined by calibrated forceps testing. The number of apoptotic neurons and degree of glial cell reaction were assessed by immunofluorescence assay. Activation of PKC‐δ and the phosphorylation of Akt were measured by western blots. CDDO improved PHN by decreasing TRPV1‐positive nociceptive neurons, the apoptotic neurons, and reversed glial cell reaction in adult rats. It also suppressed the enhanced PKC‐δ and p‐Akt signalling in the sciatic nerve, dorsal root ganglia (DRG) and spinal dorsal horn. Our research is the promising report demonstrating the analgesic and neuroprotective action of CDDO in a PHN‐rat's model by regulating central and peripheral sensitization targeting TRPV1, PKC‐δ and p‐Akt. It also is the first study to elucidate the role of oligodendrocyte in PHN.</description><identifier>ISSN: 1582-1838</identifier><identifier>ISSN: 1582-4934</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.18131</identifier><identifier>PMID: 38426931</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>AKT protein ; analgesic ; Analgesics ; Antibodies ; Apoptosis ; Capsaicin receptors ; Cell death ; Cell growth ; Dorsal horn ; Dorsal root ganglia ; Glial cells ; Herpes viruses ; Hyperalgesia ; Immunofluorescence ; Inflammation ; Kinases ; Microglia ; Nervous system ; Neuralgia ; Neuronal-glial interactions ; Neurons ; Neuroprotection ; neuroprotective ; Pain ; Pain perception ; Phosphorylation ; postherpetic neuralgia (PHN) ; Protein kinase C ; Quality of life ; Sciatic nerve ; sensitization ; Western blotting</subject><ispartof>Journal of cellular and molecular medicine, 2024-03, Vol.28 (6), p.e18131-n/a</ispartof><rights>2024 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2024 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3931-6b8fbcf6f0bcb3ce8d162ea75e72d349d0913550eeca63894462a74a0f7048db3</citedby><cites>FETCH-LOGICAL-c3931-6b8fbcf6f0bcb3ce8d162ea75e72d349d0913550eeca63894462a74a0f7048db3</cites><orcidid>0000-0001-7227-2345</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjcmm.18131$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjcmm.18131$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,860,1411,11541,27901,27902,45550,45551,46027,46451</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38426931$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Chun‐Ching</creatorcontrib><creatorcontrib>Lin, Chia‐Yang</creatorcontrib><creatorcontrib>Lu, Ying‐Yi</creatorcontrib><creatorcontrib>Tsai, Hung‐Pei</creatorcontrib><creatorcontrib>Lin, Chih‐Lung</creatorcontrib><creatorcontrib>Wu, Chieh‐Hsin</creatorcontrib><title>CDDO regulates central and peripheral sensitization to attenuate post‐herpetic neuralgia by targeting TRPV1/PKC‐δ/p‐Akt signals</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Postherpetic neuralgia (PHN) is a notorious neuropathic pain featuring persistent profound mechanical hyperalgesia with significant negative impact on patients' life quality. CDDO can regulate inflammatory response and programmed cell death. Its derivative also protects neurons from damages by modulating microglia activities. As a consequence of central and peripheral sensitization, applying neural blocks may benefit to minimize the risk of PHN. This study aimed to explore whether CDDO could generate analgesic action in a PHN‐rats' model. The behavioural test was determined by calibrated forceps testing. The number of apoptotic neurons and degree of glial cell reaction were assessed by immunofluorescence assay. Activation of PKC‐δ and the phosphorylation of Akt were measured by western blots. CDDO improved PHN by decreasing TRPV1‐positive nociceptive neurons, the apoptotic neurons, and reversed glial cell reaction in adult rats. It also suppressed the enhanced PKC‐δ and p‐Akt signalling in the sciatic nerve, dorsal root ganglia (DRG) and spinal dorsal horn. Our research is the promising report demonstrating the analgesic and neuroprotective action of CDDO in a PHN‐rat's model by regulating central and peripheral sensitization targeting TRPV1, PKC‐δ and p‐Akt. It also is the first study to elucidate the role of oligodendrocyte in PHN.</description><subject>AKT protein</subject><subject>analgesic</subject><subject>Analgesics</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Capsaicin receptors</subject><subject>Cell death</subject><subject>Cell growth</subject><subject>Dorsal horn</subject><subject>Dorsal root ganglia</subject><subject>Glial cells</subject><subject>Herpes viruses</subject><subject>Hyperalgesia</subject><subject>Immunofluorescence</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Microglia</subject><subject>Nervous system</subject><subject>Neuralgia</subject><subject>Neuronal-glial interactions</subject><subject>Neurons</subject><subject>Neuroprotection</subject><subject>neuroprotective</subject><subject>Pain</subject><subject>Pain perception</subject><subject>Phosphorylation</subject><subject>postherpetic neuralgia (PHN)</subject><subject>Protein kinase C</subject><subject>Quality of life</subject><subject>Sciatic nerve</subject><subject>sensitization</subject><subject>Western blotting</subject><issn>1582-1838</issn><issn>1582-4934</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kctO3DAUhq2KqsDQTR-gssQGIQ3jSy7OEmWAXkCginYbOc5J6mniBNsRGlasWPdh-hx9iD5Jnc6URRc9m__Y-s6vo_Mj9IaSExpqsVJdd0IF5fQF2qOxYPMo49HOtqeCi12079yKEJ5Qnr1Cu1xELMk43UNP-XJ5jS00Yys9OKzAeCtbLE2FB7B6-ArT04Fx2usH6XVvsO-x9B7MGEbw0Dv_6_F74AbwWmEDY5hotMTlGntpm_BrGnz76eYLXdx8zAP788diCHL6zWOnGyNbd4Be1kHg9VZn6PP52W3-bn55ffE-P72cKx7WnSelqEtVJzUpVckViIomDGQaQ8oqHmUVySiPYwKgZMJFFkUJk2kkSZ2SSFQln6Gjje9g-7sRnC867RS0rTTQj65g4XAsZWk4zgwd_oOu-tFOywYqTmmSMTpRxxtK2d45C3UxWN1Juy4oKaZ0iimd4k86AX67tRzLDqpn9G8cAaAb4F63sP6PVfEhv7ramP4G0NOe0w</recordid><startdate>202403</startdate><enddate>202403</enddate><creator>Lu, 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and peripheral sensitization to attenuate post‐herpetic neuralgia by targeting TRPV1/PKC‐δ/p‐Akt signals</title><author>Lu, Chun‐Ching ; Lin, Chia‐Yang ; Lu, Ying‐Yi ; Tsai, Hung‐Pei ; Lin, Chih‐Lung ; Wu, Chieh‐Hsin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3931-6b8fbcf6f0bcb3ce8d162ea75e72d349d0913550eeca63894462a74a0f7048db3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>AKT protein</topic><topic>analgesic</topic><topic>Analgesics</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Capsaicin receptors</topic><topic>Cell death</topic><topic>Cell growth</topic><topic>Dorsal horn</topic><topic>Dorsal root ganglia</topic><topic>Glial cells</topic><topic>Herpes viruses</topic><topic>Hyperalgesia</topic><topic>Immunofluorescence</topic><topic>Inflammation</topic><topic>Kinases</topic><topic>Microglia</topic><topic>Nervous system</topic><topic>Neuralgia</topic><topic>Neuronal-glial interactions</topic><topic>Neurons</topic><topic>Neuroprotection</topic><topic>neuroprotective</topic><topic>Pain</topic><topic>Pain perception</topic><topic>Phosphorylation</topic><topic>postherpetic neuralgia (PHN)</topic><topic>Protein kinase C</topic><topic>Quality of life</topic><topic>Sciatic nerve</topic><topic>sensitization</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lu, Chun‐Ching</creatorcontrib><creatorcontrib>Lin, Chia‐Yang</creatorcontrib><creatorcontrib>Lu, Ying‐Yi</creatorcontrib><creatorcontrib>Tsai, Hung‐Pei</creatorcontrib><creatorcontrib>Lin, Chih‐Lung</creatorcontrib><creatorcontrib>Wu, Chieh‐Hsin</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue 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Med</addtitle><date>2024-03</date><risdate>2024</risdate><volume>28</volume><issue>6</issue><spage>e18131</spage><epage>n/a</epage><pages>e18131-n/a</pages><issn>1582-1838</issn><issn>1582-4934</issn><eissn>1582-4934</eissn><abstract>Postherpetic neuralgia (PHN) is a notorious neuropathic pain featuring persistent profound mechanical hyperalgesia with significant negative impact on patients' life quality. CDDO can regulate inflammatory response and programmed cell death. Its derivative also protects neurons from damages by modulating microglia activities. As a consequence of central and peripheral sensitization, applying neural blocks may benefit to minimize the risk of PHN. This study aimed to explore whether CDDO could generate analgesic action in a PHN‐rats' model. The behavioural test was determined by calibrated forceps testing. The number of apoptotic neurons and degree of glial cell reaction were assessed by immunofluorescence assay. Activation of PKC‐δ and the phosphorylation of Akt were measured by western blots. CDDO improved PHN by decreasing TRPV1‐positive nociceptive neurons, the apoptotic neurons, and reversed glial cell reaction in adult rats. It also suppressed the enhanced PKC‐δ and p‐Akt signalling in the sciatic nerve, dorsal root ganglia (DRG) and spinal dorsal horn. Our research is the promising report demonstrating the analgesic and neuroprotective action of CDDO in a PHN‐rat's model by regulating central and peripheral sensitization targeting TRPV1, PKC‐δ and p‐Akt. It also is the first study to elucidate the role of oligodendrocyte in PHN.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>38426931</pmid><doi>10.1111/jcmm.18131</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-7227-2345</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | AKT protein analgesic Analgesics Antibodies Apoptosis Capsaicin receptors Cell death Cell growth Dorsal horn Dorsal root ganglia Glial cells Herpes viruses Hyperalgesia Immunofluorescence Inflammation Kinases Microglia Nervous system Neuralgia Neuronal-glial interactions Neurons Neuroprotection neuroprotective Pain Pain perception Phosphorylation postherpetic neuralgia (PHN) Protein kinase C Quality of life Sciatic nerve sensitization Western blotting |
title | CDDO regulates central and peripheral sensitization to attenuate post‐herpetic neuralgia by targeting TRPV1/PKC‐δ/p‐Akt signals |
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