Decursin Alleviates Mechanical Allodynia in a Paclitaxel-Induced Neuropathic Pain Mouse Model
DC Field | Value | Language |
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dc.contributor.author | Son, Dang Bao | - |
dc.contributor.author | Choi, Woosik | - |
dc.contributor.author | Kim, Mingu | - |
dc.contributor.author | Go, Eun Jin | - |
dc.contributor.author | Jeong, Dabeen | - |
dc.contributor.author | Park, Chul-Kyu | - |
dc.contributor.author | Kim, Yong Ho | - |
dc.contributor.author | Lee, Hanki | - |
dc.contributor.author | Suh, Joo-Won | - |
dc.date.available | 2021-04-05T01:40:25Z | - |
dc.date.created | 2021-04-05 | - |
dc.date.issued | 2021-03 | - |
dc.identifier.issn | 2073-4409 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/80637 | - |
dc.description.abstract | Chemotherapy-induced neuropathic pain (CINP) is a severe adverse effect of platinum- and taxane-derived anticancer drugs. The pathophysiology of CINP includes damage to neuronal networks and dysregulation of signal transduction due to abnormal Ca2+ levels. Therefore, methods that aid the recovery of neuronal networks could represent a potential treatment for CINP. We developed a mouse model of paclitaxel-induced peripheral neuropathy, representing CINP, to examine whether intrathecal injection of decursin could be effective in treating CINP. We found that decursin reduced capsaicin-induced intracellular Ca2+ levels in F11 cells and stimulated neurite outgrowth in a concentration-dependent manner. Decursin directly reduced mechanical allodynia, and this improvement was even greater with a higher frequency of injections. Subsequently, we investigated whether decursin interacts with the transient receptor potential vanilloid 1 (TRPV1). The web server SwissTargetPrediction predicted that TRPV1 is one of the target proteins that may enable the effective treatment of CINP. Furthermore, we discovered that decursin acts as a TRPV1 antagonist. Therefore, we demonstrated that decursin may be an important compound for the treatment of paclitaxel-induced neuropathic pain that functions via TRPV1 inhibition and recovery of damaged neuronal networks. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | MDPI | - |
dc.relation.isPartOf | CELLS | - |
dc.title | Decursin Alleviates Mechanical Allodynia in a Paclitaxel-Induced Neuropathic Pain Mouse Model | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000633467900001 | - |
dc.identifier.doi | 10.3390/cells10030547 | - |
dc.identifier.bibliographicCitation | CELLS, v.10, no.3 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.scopusid | 2-s2.0-85103862988 | - |
dc.citation.title | CELLS | - |
dc.citation.volume | 10 | - |
dc.citation.number | 3 | - |
dc.contributor.affiliatedAuthor | Kim, Mingu | - |
dc.contributor.affiliatedAuthor | Go, Eun Jin | - |
dc.contributor.affiliatedAuthor | Park, Chul-Kyu | - |
dc.contributor.affiliatedAuthor | Kim, Yong Ho | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | CINP | - |
dc.subject.keywordAuthor | decursin | - |
dc.subject.keywordAuthor | recovery of damaged neuronal network | - |
dc.subject.keywordAuthor | TRPV1 antagonist | - |
dc.subject.keywordAuthor | lead compound | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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