Lidocaine Alleviates Neuropathic Pain and Neuroinflammation by Inhibiting HMGB1 Expression to Mediate MIP-1α/CCR1 Pathway
High mobility group box 1 (HMGB1) released from sensory nerve tissues can induce neuropathic pain. Whether HMGB1 is implicated in the mechanism underlying the effect of lidocaine in pain management remains to be determined. This study aims to explore the effect of lidocaine in a rat model of spared...
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| Veröffentlicht in: | Journal of neuroimmune pharmacology 2021-06, Vol.16 (2), p.318-333 |
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| creator | Li, Mingming Jiang, Hao Gu, Kuo Sun, Xuechao Gu, Jing Li, Chunming Wang, Guonian |
| description | High mobility group box 1 (HMGB1) released from sensory nerve tissues can induce neuropathic pain. Whether HMGB1 is implicated in the mechanism underlying the effect of lidocaine in pain management remains to be determined. This study aims to explore the effect of lidocaine in a rat model of spared nerve injury (SNI) and the underlying mechanism. An SNI model was established via nerve ligation. Two weeks after the SNI model was established, rats were intrathecally injected with lidocaine, an HMGB1 antibody (HMG Ab), an MIP-1α antibody (MIP-1α Ab), a CCR1 inhibitor (CCR1-RS) or a CCR5 antagonist (CCR5-Mar). Pain behaviors were assessed before and after model establishment to calculate the number of spontaneous flinches (NSF), paw withdrawal threshold (PWT), paw withdrawal thermal latency (PWL) and sciatic function index (SFI). Cell apoptosis and the inflammatory response in the cerebrospinal fluid (CSF) were detected by TUNEL staining and ELISA. The mRNA and protein expression levels of MIP-1α, CCR1 and CCR5 were determined by RT-PCR and Western blotting. The expression levels of HMGB1, MIP-1α, CCR1 and CCR5 were measured by Western blotting and immunofluorescence. Pain behavior testing in SNI rats showed that SNI rats exhibited an increased NSF and a decreased PWT, PWL and SFI. Cell apoptosis in the spinal dorsal horn and the generation of inflammatory cytokines were enhanced in SNI rats, and the expression levels of HMGB1, MIP-1α, CCR1 and CCR5 were upregulated. HMGB1 cytoplasmic translocation, the coexpression of MIP-1α with NeuN, and the coexpression of CCR1 and CCR5 with OX42 were also observed in SNI rats. Neuropathic pain and neuroinflammation were suppressed by the intrathecal injection of lidocaine, HMG Ab, MIP-1α Ab, CCR1-RS or CCR5-Mar. Lidocaine inhibited the expression levels of HMGB1, MIP-1α, CCR1 and CCR5, and the HMGB1 antibody suppressed the expression of MIP-1α, CCR1 and CCR5. Lidocaine attenuates neuropathic pain and neuroinflammation by inhibiting HMGB1 to regulate the MIP-1α/CCR1/CCR5 pathway.
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| doi_str_mv | 10.1007/s11481-020-09913-y |
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Graphical Abstract</description><identifier>ISSN: 1557-1890</identifier><identifier>EISSN: 1557-1904</identifier><identifier>DOI: 10.1007/s11481-020-09913-y</identifier><identifier>PMID: 32301050</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Antibodies ; Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Immunology ; Neurosciences ; Original Article ; Pain ; Pharmacology/Toxicology ; Virology</subject><ispartof>Journal of neuroimmune pharmacology, 2021-06, Vol.16 (2), p.318-333</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-60edc5fd5c7b7e2f1e4316e83f45f99459313764470275dea79569a9d65eade3</citedby><cites>FETCH-LOGICAL-c375t-60edc5fd5c7b7e2f1e4316e83f45f99459313764470275dea79569a9d65eade3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11481-020-09913-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11481-020-09913-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32301050$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Mingming</creatorcontrib><creatorcontrib>Jiang, Hao</creatorcontrib><creatorcontrib>Gu, Kuo</creatorcontrib><creatorcontrib>Sun, Xuechao</creatorcontrib><creatorcontrib>Gu, Jing</creatorcontrib><creatorcontrib>Li, Chunming</creatorcontrib><creatorcontrib>Wang, Guonian</creatorcontrib><title>Lidocaine Alleviates Neuropathic Pain and Neuroinflammation by Inhibiting HMGB1 Expression to Mediate MIP-1α/CCR1 Pathway</title><title>Journal of neuroimmune pharmacology</title><addtitle>J Neuroimmune Pharmacol</addtitle><addtitle>J Neuroimmune Pharmacol</addtitle><description>High mobility group box 1 (HMGB1) released from sensory nerve tissues can induce neuropathic pain. Whether HMGB1 is implicated in the mechanism underlying the effect of lidocaine in pain management remains to be determined. This study aims to explore the effect of lidocaine in a rat model of spared nerve injury (SNI) and the underlying mechanism. An SNI model was established via nerve ligation. Two weeks after the SNI model was established, rats were intrathecally injected with lidocaine, an HMGB1 antibody (HMG Ab), an MIP-1α antibody (MIP-1α Ab), a CCR1 inhibitor (CCR1-RS) or a CCR5 antagonist (CCR5-Mar). Pain behaviors were assessed before and after model establishment to calculate the number of spontaneous flinches (NSF), paw withdrawal threshold (PWT), paw withdrawal thermal latency (PWL) and sciatic function index (SFI). Cell apoptosis and the inflammatory response in the cerebrospinal fluid (CSF) were detected by TUNEL staining and ELISA. The mRNA and protein expression levels of MIP-1α, CCR1 and CCR5 were determined by RT-PCR and Western blotting. The expression levels of HMGB1, MIP-1α, CCR1 and CCR5 were measured by Western blotting and immunofluorescence. Pain behavior testing in SNI rats showed that SNI rats exhibited an increased NSF and a decreased PWT, PWL and SFI. Cell apoptosis in the spinal dorsal horn and the generation of inflammatory cytokines were enhanced in SNI rats, and the expression levels of HMGB1, MIP-1α, CCR1 and CCR5 were upregulated. HMGB1 cytoplasmic translocation, the coexpression of MIP-1α with NeuN, and the coexpression of CCR1 and CCR5 with OX42 were also observed in SNI rats. Neuropathic pain and neuroinflammation were suppressed by the intrathecal injection of lidocaine, HMG Ab, MIP-1α Ab, CCR1-RS or CCR5-Mar. Lidocaine inhibited the expression levels of HMGB1, MIP-1α, CCR1 and CCR5, and the HMGB1 antibody suppressed the expression of MIP-1α, CCR1 and CCR5. Lidocaine attenuates neuropathic pain and neuroinflammation by inhibiting HMGB1 to regulate the MIP-1α/CCR1/CCR5 pathway.
Graphical Abstract</description><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Immunology</subject><subject>Neurosciences</subject><subject>Original Article</subject><subject>Pain</subject><subject>Pharmacology/Toxicology</subject><subject>Virology</subject><issn>1557-1890</issn><issn>1557-1904</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp9kctu1DAUhi0EoqXwAiyQJTZsQo9v8XhZRr2MNAMV6t7yxCcdV4kzxAmQvhUvwjPhIS1ILFjZ8v-d35Y_Ql4zeM8A9GliTC5YARwKMIaJYnpCjplSumAG5NPH_cLAEXmR0h2AlBLgOTkSXAADBcfkfh18V7kQkZ41DX4NbsBEP-LYd3s37EJFr3NIXfTzYYh149rWDaGLdDvRVdyFbRhCvKVXm8sPjJ5_3_eY0iEeOrpBf2ikm9V1wX7-OF0uP7PcOOy-uekleVa7JuGrh_WE3Fyc3yyvivWny9XybF1UQquhKAF9pWqvKr3VyGuGUrASF6KWqjZGKiOY0KWUGrhWHp02qjTO-FKh8yhOyLu5dt93X0ZMg21DqrBpXMRuTJYLw4wWhi8y-vYf9K4b-5gfZ7nikD8MOM8Un6mq71Lqsbb7PrSunywDexBjZzE2i7G_xdgpD715qB63Lfo_I48mMiBmIOUo3mL_9-7_1P4CjFCYzQ</recordid><startdate>20210601</startdate><enddate>20210601</enddate><creator>Li, Mingming</creator><creator>Jiang, Hao</creator><creator>Gu, Kuo</creator><creator>Sun, Xuechao</creator><creator>Gu, Jing</creator><creator>Li, Chunming</creator><creator>Wang, Guonian</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20210601</creationdate><title>Lidocaine Alleviates Neuropathic Pain and Neuroinflammation by Inhibiting HMGB1 Expression to Mediate MIP-1α/CCR1 Pathway</title><author>Li, Mingming ; Jiang, Hao ; Gu, Kuo ; Sun, Xuechao ; Gu, Jing ; Li, Chunming ; Wang, Guonian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-60edc5fd5c7b7e2f1e4316e83f45f99459313764470275dea79569a9d65eade3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Immunology</topic><topic>Neurosciences</topic><topic>Original Article</topic><topic>Pain</topic><topic>Pharmacology/Toxicology</topic><topic>Virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Mingming</creatorcontrib><creatorcontrib>Jiang, Hao</creatorcontrib><creatorcontrib>Gu, Kuo</creatorcontrib><creatorcontrib>Sun, Xuechao</creatorcontrib><creatorcontrib>Gu, Jing</creatorcontrib><creatorcontrib>Li, Chunming</creatorcontrib><creatorcontrib>Wang, Guonian</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neuroimmune pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Mingming</au><au>Jiang, Hao</au><au>Gu, Kuo</au><au>Sun, Xuechao</au><au>Gu, Jing</au><au>Li, Chunming</au><au>Wang, Guonian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lidocaine Alleviates Neuropathic Pain and Neuroinflammation by Inhibiting HMGB1 Expression to Mediate MIP-1α/CCR1 Pathway</atitle><jtitle>Journal of neuroimmune pharmacology</jtitle><stitle>J Neuroimmune Pharmacol</stitle><addtitle>J Neuroimmune Pharmacol</addtitle><date>2021-06-01</date><risdate>2021</risdate><volume>16</volume><issue>2</issue><spage>318</spage><epage>333</epage><pages>318-333</pages><issn>1557-1890</issn><eissn>1557-1904</eissn><abstract>High mobility group box 1 (HMGB1) released from sensory nerve tissues can induce neuropathic pain. Whether HMGB1 is implicated in the mechanism underlying the effect of lidocaine in pain management remains to be determined. This study aims to explore the effect of lidocaine in a rat model of spared nerve injury (SNI) and the underlying mechanism. An SNI model was established via nerve ligation. Two weeks after the SNI model was established, rats were intrathecally injected with lidocaine, an HMGB1 antibody (HMG Ab), an MIP-1α antibody (MIP-1α Ab), a CCR1 inhibitor (CCR1-RS) or a CCR5 antagonist (CCR5-Mar). Pain behaviors were assessed before and after model establishment to calculate the number of spontaneous flinches (NSF), paw withdrawal threshold (PWT), paw withdrawal thermal latency (PWL) and sciatic function index (SFI). Cell apoptosis and the inflammatory response in the cerebrospinal fluid (CSF) were detected by TUNEL staining and ELISA. The mRNA and protein expression levels of MIP-1α, CCR1 and CCR5 were determined by RT-PCR and Western blotting. The expression levels of HMGB1, MIP-1α, CCR1 and CCR5 were measured by Western blotting and immunofluorescence. Pain behavior testing in SNI rats showed that SNI rats exhibited an increased NSF and a decreased PWT, PWL and SFI. Cell apoptosis in the spinal dorsal horn and the generation of inflammatory cytokines were enhanced in SNI rats, and the expression levels of HMGB1, MIP-1α, CCR1 and CCR5 were upregulated. HMGB1 cytoplasmic translocation, the coexpression of MIP-1α with NeuN, and the coexpression of CCR1 and CCR5 with OX42 were also observed in SNI rats. Neuropathic pain and neuroinflammation were suppressed by the intrathecal injection of lidocaine, HMG Ab, MIP-1α Ab, CCR1-RS or CCR5-Mar. Lidocaine inhibited the expression levels of HMGB1, MIP-1α, CCR1 and CCR5, and the HMGB1 antibody suppressed the expression of MIP-1α, CCR1 and CCR5. Lidocaine attenuates neuropathic pain and neuroinflammation by inhibiting HMGB1 to regulate the MIP-1α/CCR1/CCR5 pathway.
Graphical Abstract</abstract><cop>New York</cop><pub>Springer US</pub><pmid>32301050</pmid><doi>10.1007/s11481-020-09913-y</doi><tpages>16</tpages></addata></record> |
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| subjects | Antibodies Apoptosis Biomedical and Life Sciences Biomedicine Cell Biology Immunology Neurosciences Original Article Pain Pharmacology/Toxicology Virology |
| title | Lidocaine Alleviates Neuropathic Pain and Neuroinflammation by Inhibiting HMGB1 Expression to Mediate MIP-1α/CCR1 Pathway |
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