Botulinum toxin type A promotes microglial M2 polarization and suppresses chronic constriction injury-induced neuropathic pain through the P2X7 receptor
Abstract Background Switching microglial polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype represents a novel therapeutic strategy for neuropathic pain (NP). This study aims to investigate whether botulinum toxin type A (BTX-A) regulates microglial M1/M2 polar...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2020-03-01
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| Series: | Cell & Bioscience |
| Subjects: | |
| Online Access: | http://link.springer.com/article/10.1186/s13578-020-00405-3 |
| _version_ | 1828521606268321792 |
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| author | Xianwei Gui Hansen Wang Lanxiang Wu Sheng Tian Xuan Wang Heqing Zheng Wei Wu |
| author_facet | Xianwei Gui Hansen Wang Lanxiang Wu Sheng Tian Xuan Wang Heqing Zheng Wei Wu |
| author_sort | Xianwei Gui |
| collection | DOAJ |
| description | Abstract Background Switching microglial polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype represents a novel therapeutic strategy for neuropathic pain (NP). This study aims to investigate whether botulinum toxin type A (BTX-A) regulates microglial M1/M2 polarization by inhibiting P2X7 expression in a rat model of NP. Results The BTX-A administration elevated pain threshold, induced microglial polarization toward the M2 phenotype, and decreased P2X7 protein level in a rat model of NP induced by chronic compression injury (CCI). Lipopolysaccharide (LPS) was used to activate HAPI rat microglial cells as an in vitro inflammatory model and we demonstrated that BTX-A promoted microglial M2 polarization in LPS-stimulated HAPI microglial cells through suppressing P2X7. Conclusions Our results indicate that BTX-A promotes microglial M2 polarization and suppresses CCI-induced NP through inhibiting P2X7 receptor. These findings provide new insights into the mechanism of BTX-A in relieving NP. |
| first_indexed | 2024-12-11T19:53:06Z |
| format | Article |
| id | doaj.art-a8444d586ff24f28a9c4e0607ec27951 |
| institution | Directory Open Access Journal |
| issn | 2045-3701 |
| language | English |
| last_indexed | 2024-12-11T19:53:06Z |
| publishDate | 2020-03-01 |
| publisher | BMC |
| record_format | Article |
| series | Cell & Bioscience |
| spelling | doaj.art-a8444d586ff24f28a9c4e0607ec279512022-12-22T00:52:44ZengBMCCell & Bioscience2045-37012020-03-0110111010.1186/s13578-020-00405-3Botulinum toxin type A promotes microglial M2 polarization and suppresses chronic constriction injury-induced neuropathic pain through the P2X7 receptorXianwei Gui0Hansen Wang1Lanxiang Wu2Sheng Tian3Xuan Wang4Heqing Zheng5Wei Wu6Department of Neurology, The Second Affiliated Hospital of Nanchang UniversityDepartment of Neurology, The Second Affiliated Hospital of Nanchang UniversityDepartment of Neurology, The Second Affiliated Hospital of Nanchang UniversityDepartment of Neurology, The Second Affiliated Hospital of Nanchang UniversityDepartment of Neurology, The Second Affiliated Hospital of Nanchang UniversityDepartment of Neurology, The Second Affiliated Hospital of Nanchang UniversityDepartment of Neurology, The Second Affiliated Hospital of Nanchang UniversityAbstract Background Switching microglial polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype represents a novel therapeutic strategy for neuropathic pain (NP). This study aims to investigate whether botulinum toxin type A (BTX-A) regulates microglial M1/M2 polarization by inhibiting P2X7 expression in a rat model of NP. Results The BTX-A administration elevated pain threshold, induced microglial polarization toward the M2 phenotype, and decreased P2X7 protein level in a rat model of NP induced by chronic compression injury (CCI). Lipopolysaccharide (LPS) was used to activate HAPI rat microglial cells as an in vitro inflammatory model and we demonstrated that BTX-A promoted microglial M2 polarization in LPS-stimulated HAPI microglial cells through suppressing P2X7. Conclusions Our results indicate that BTX-A promotes microglial M2 polarization and suppresses CCI-induced NP through inhibiting P2X7 receptor. These findings provide new insights into the mechanism of BTX-A in relieving NP.http://link.springer.com/article/10.1186/s13578-020-00405-3Botulinum toxin type ANeuropathic painMicrogliaM1/M2 polarizationP2X7 receptor |
| spellingShingle | Xianwei Gui Hansen Wang Lanxiang Wu Sheng Tian Xuan Wang Heqing Zheng Wei Wu Botulinum toxin type A promotes microglial M2 polarization and suppresses chronic constriction injury-induced neuropathic pain through the P2X7 receptor Cell & Bioscience Botulinum toxin type A Neuropathic pain Microglia M1/M2 polarization P2X7 receptor |
| title | Botulinum toxin type A promotes microglial M2 polarization and suppresses chronic constriction injury-induced neuropathic pain through the P2X7 receptor |
| title_full | Botulinum toxin type A promotes microglial M2 polarization and suppresses chronic constriction injury-induced neuropathic pain through the P2X7 receptor |
| title_fullStr | Botulinum toxin type A promotes microglial M2 polarization and suppresses chronic constriction injury-induced neuropathic pain through the P2X7 receptor |
| title_full_unstemmed | Botulinum toxin type A promotes microglial M2 polarization and suppresses chronic constriction injury-induced neuropathic pain through the P2X7 receptor |
| title_short | Botulinum toxin type A promotes microglial M2 polarization and suppresses chronic constriction injury-induced neuropathic pain through the P2X7 receptor |
| title_sort | botulinum toxin type a promotes microglial m2 polarization and suppresses chronic constriction injury induced neuropathic pain through the p2x7 receptor |
| topic | Botulinum toxin type A Neuropathic pain Microglia M1/M2 polarization P2X7 receptor |
| url | http://link.springer.com/article/10.1186/s13578-020-00405-3 |
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