{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang X"],"funding":["Natural Science Foundation of Jiangxi Province","National Natural Science Foundation of China"],"pagination":["141"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7724852"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(1)"],"pubmed_abstract":["<h4>Background</h4>Botulinum toxin type A (BTX-A) was considered to be a new potential drug for neuropathic pain (NP) treatment.<h4>Results</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"],"journal":["Cell & bioscience"],"pubmed_title":["Botulinum toxin type A alleviates neuropathic pain and suppresses inflammatory cytokines release from microglia by targeting TLR2/MyD88 and SNAP23."],"pmcid":["PMC7724852"],"funding_grant_id":["20192BAB205047","31860293"],"pubmed_authors":["Zheng H","Wu L","Liu P","Tian S","Liu Q","Wang X","Wang H","Wu W"],"additional_accession":[]},"is_claimable":false,"name":"Botulinum toxin type A alleviates neuropathic pain and suppresses inflammatory cytokines release from microglia by targeting TLR2/MyD88 and SNAP23.","description":"<h4>Background</h4>Botulinum toxin type A (BTX-A) was considered to be a new potential drug for neuropathic pain (NP) treatment.<h4>Results</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","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Dec","modification":"2025-04-27T02:58:23.859Z","creation":"2025-04-06T18:39:08.953Z"},"accession":"S-EPMC7724852","cross_references":{"pubmed":["33298171"],"doi":["10.1186/s13578-020-00501-4"]}}