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

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Autor(es): dc.creatorSilva Júnior, Cláudio Antônio da-
Autor(es): dc.creatorCastro Junior, Célio José de-
Autor(es): dc.creatorPereira, Elizete Maria Rita-
Autor(es): dc.creatorBinda, Nancy Scardua-
Autor(es): dc.creatorSilva, Juliana Figueira da-
Autor(es): dc.creatorCordeiro, Marta do Nascimento-
Autor(es): dc.creatorDiniz, Danuza Montijo-
Autor(es): dc.creatorSanta Cecília, Flávia Viana-
Autor(es): dc.creatorFerreira, Juliano-
Autor(es): dc.creatorGomez, Marcus Vinicius-
Data de aceite: dc.date.accessioned2025-08-21T15:38:18Z-
Data de disponibilização: dc.date.available2025-08-21T15:38:18Z-
Data de envio: dc.date.issued2020-05-22-
Data de envio: dc.date.issued2020-05-22-
Data de envio: dc.date.issued2019-
Fonte completa do material: dc.identifierhttp://www.repositorio.ufop.br/handle/123456789/12244-
Fonte completa do material: dc.identifierhttps://link.springer.com/article/10.1007/s43440-019-00002-3-
Fonte completa do material: dc.identifierhttps://doi.org/10.1007/s43440-019-00002-3-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/capes/1020359-
Descrição: dc.descriptionBackground: 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 Phα1β, ω-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 Phα1β intrathecal (it), ω-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. Phα1β (100 pmol/it) or AMD3100 (2.5 µg/ip) reduced this hypersensitivity after 2 h treatments, while ω-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: Phα1β, ω-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 Phα1β or AMD-3100, while ω-conotoxin MVIIA did not affect. The inhibitory effects of Phα1β on PDN may involve voltage-dependent calcium channels.-
Formato: dc.formatapplication/pdf-
Idioma: dc.languageen-
Direitos: dc.rightsrestrito-
Palavras-chave: dc.subjectω-Conotoxin MVIIA-
Título: dc.titleThe inhibitory efect of Phα1β toxin on diabetic neuropathic pain involves the CXCR4 chemokine receptor.-
Aparece nas coleções:Repositório Institucional - UFOP

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