The inhibitory effect of Phα1β toxin on diabetic neuropathic pain involves the CXCR4 chemokine receptor

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dc.contributorLEDS - Laboratório de Dor e Sinalizaçãopt_BR
dc.contributor.authorJunior, Claudio Antonio da Silvapt_BR
dc.contributor.authorJunior, Célio José de Castropt_BR
dc.contributor.authorPereira, Elizete Maria Ritapt_BR
dc.contributor.authorBinda, Nancy Scarduapt_BR
dc.contributor.authorSilva, Juliana Figueira dapt_BR
dc.contributor.authorCordeiro, Marta do Nascimentopt_BR
dc.contributor.authorDiniz, Danuza Montijopt_BR
dc.contributor.authorSanta-Cecília, Flávia Vianapt_BR
dc.contributor.authorFerreira, Julianopt_BR
dc.contributor.authorGomez, Marcus Viniciuspt_BR
dc.identifier.citationJunior CAS, Junior CJC, Pereira EMR, Binda NS, Silva JF, Cordeiro MN, et al. The inhibitory effect of Pha1ß toxin on diabetic neuropathic pain involves the CXCR4 chemokine receptor. Pharmacol Rep. 2020 Jan;72:47-54. doi:10.1007/s43440-019-00002-3.pt_BR
dc.description.abstractBackground Diabetic neuropathy is a common cause of painful diabetic neuropathy (PDN). C-X-C chemokine receptor type 4 (CXCR4) expression is increased in peripheral nerve samples from diabetes patients, suggesting a role for CXCR4 in PDN. Therefore, we evaluated the effects of Pha1ß, Ômega-conotoxin MVIIA, and AMD3100 in a model of streptozotocin (STZ)-induced PDN in rodents and naïve model of rats with the activation of the CXCR4/stromal cell-derived factor 1 (SDF-1) signal. Methods Diabetic neuropathy was induced by intraperitoneal (ip) injection of STZ in Wistar rats. Naïve rats were intrathecally injected with SDF-1 to test the CXCR4/SDF-1 signal. The effects of Pha1ß intrathecal (it), Ômega-conotoxin MVIIA intrathecal (it), and AMD3100 intraperitoneal (ip) on rat hypersensitivity, IL-6, and the intracellular calcium [Ca2+]i content of diabetic synaptosomes were studied. Results The drugs reduced the hypersensitivity in diabetic rats. SDF-1 (1.0 µg/it) administration in naïve rats induced hypersensitivity. Pha1ß (100 pmol/it) or AMD3100 (2.5 µg/ip) reduced this hypersensitivity after 2 h treatments, while Ômega-conotoxin MVIIA did not have an effect. IL-6 and [Ca2+]i content increased in the spinal cord synaptosomes in diabetic rats. The drug treatments reduced IL-6 and the calcium influx in diabetic synaptosomes. Conclusions Pha1ß, Ômega-conotoxin MVIIA, and AMD3100, after 2 h of treatment of STZ-induced PDN, reduced hypersensitivity in diabetic rats. In naïve rats with CXCR4/SDF-1 activation, the induced hypersensitivity decreased after 2 h treatments with Pha1ß or AMD-3100, while Ômega-conotoxin MVIIA did not affect. The inhibitory effects of Pha1ß on PDN may involve voltage-dependent calcium channels.pt_BR
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG)pt_BR
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt_BR
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)pt_BR
dc.relation.ispartofPharmacological Reportspt_BR
dc.titleThe inhibitory effect of Phα1β toxin on diabetic neuropathic pain involves the CXCR4 chemokine receptorpt_BR
dc.contributor.externalSanta Casa BH Ensino e Pesquisa (SCBH)¦¦Brasilpt_BR
dc.contributor.externalFundação Ezequiel Dias (FUNED)¦¦Brasilpt_BR
dc.contributor.externalUniversidade Federal de Santa Catarina¦¦Brasilpt_BR
dc.subject.keywordDiabetic neuropathypt_BR
dc.subject.keywordômega-Conotoxin MVIIApt_BR
dc.subject.keywordCXCR4 chemokine receptorpt_BR
dc.relation.ispartofabbreviatedPharmacol Reppt_BR
dc.identifier.citationabntv. 72, p. 47-54, jan. 2020pt_BR
dc.identifier.citationvancouver2020 Jan;72:47-54pt_BR
dc.contributor.butantanSanta-Cecília, Flávia Viana|:Aluno|:LEDS - Laboratório de Dor e Sinalização|:pt_BR
dc.sponsorship.butantanConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)¦¦pt_BR
dc.sponsorship.butantanCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)¦¦pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG)¦¦pt_BR
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