<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wang X</submitter><funding>Natural Science Foundation of Jiangxi Province</funding><funding>National Natural Science Foundation of China</funding><pagination>141</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7724852</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Botulinum toxin type A (BTX-A) was considered to be a new potential drug for neuropathic pain (NP) treatment.&lt;h4>Results&lt;/h4>In vivo, BTX-A attenuated chronic compression injury (CCI)-induced pain in rats, and reduced production of pro-inflammatory factors. The inhibition of BTX-A to expression and phosphorylation of SNAP23 were partly reversed by TLR2/MyD88 upregulation. In LPS-stimulated microglia, we also found that BTX-A suppressed TLR2, MyD88, p-SNAP23 and SNAP23 expression, and reduced pro-inflammatory factors secretion. Upregulation of TLR2 and MyD88 recued the inhibition of BTX-A to LPS-induced activation of SNAP23. Then, we demonstrated that BTX-A reduced expression of SNAP23 through inhibition of IKKα/β phosphorylation. Besides, the inhibition of BTX-A to LPS-i</pubmed_abstract><journal>Cell &amp; bioscience</journal><pubmed_title>Botulinum toxin type A alleviates neuropathic pain and suppresses inflammatory cytokines release from microglia by targeting TLR2/MyD88 and SNAP23.</pubmed_title><pmcid>PMC7724852</pmcid><funding_grant_id>20192BAB205047</funding_grant_id><funding_grant_id>31860293</funding_grant_id><pubmed_authors>Zheng H</pubmed_authors><pubmed_authors>Wu L</pubmed_authors><pubmed_authors>Liu P</pubmed_authors><pubmed_authors>Tian S</pubmed_authors><pubmed_authors>Liu Q</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Wang H</pubmed_authors><pubmed_authors>Wu W</pubmed_authors></additional><is_claimable>false</is_claimable><name>Botulinum toxin type A alleviates neuropathic pain and suppresses inflammatory cytokines release from microglia by targeting TLR2/MyD88 and SNAP23.</name><description>&lt;h4>Background&lt;/h4>Botulinum toxin type A (BTX-A) was considered to be a new potential drug for neuropathic pain (NP) treatment.&lt;h4>Results&lt;/h4>In vivo, BTX-A attenuated chronic compression injury (CCI)-induced pain in rats, and reduced production of pro-inflammatory factors. The inhibition of BTX-A to expression and phosphorylation of SNAP23 were partly reversed by TLR2/MyD88 upregulation. In LPS-stimulated microglia, we also found that BTX-A suppressed TLR2, MyD88, p-SNAP23 and SNAP23 expression, and reduced pro-inflammatory factors secretion. Upregulation of TLR2 and MyD88 recued the inhibition of BTX-A to LPS-induced activation of SNAP23. Then, we demonstrated that BTX-A reduced expression of SNAP23 through inhibition of IKKα/β phosphorylation. Besides, the inhibition of BTX-A to LPS-i</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Dec</publication><modification>2025-04-27T02:58:23.859Z</modification><creation>2025-04-06T18:39:08.953Z</creation></dates><accession>S-EPMC7724852</accession><cross_references><pubmed>33298171</pubmed><doi>10.1186/s13578-020-00501-4</doi></cross_references></HashMap>