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Repurposing of the Nootropic Drug Vinpocetine as an Analgesic and Anti-Inflammatory Agent: Evidence in a Mouse Model of Superoxide Anion-Triggered Inflammation

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Autor(es):
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Lourenco-Gonzalez, Yuri [1] ; Fattori, Victor [1] ; Domiciano, Talita P. [2] ; Rossaneis, Ana C. [1] ; Borghi, Sergio M. [1] ; Zaninelli, Tiago H. [1] ; Bernardy, Catia C. F. [3] ; Alves-Filho, Jose C. [2] ; Cunha, Thiago M. [2] ; Cunha, Fernando Q. [2] ; Casagrande, Rubia [4] ; Verri Jr, Waldiceu A.
Número total de Autores: 12
Afiliação do(s) autor(es):
[1] Univ Estadual Londrina, Dept Ciencias Patol, Ctr Ciencias Biol, Rod Celso Garcia Cid Km 480 PR 445, Londrina, Parana - Brazil
[2] Univ Sao Paulo, Dept Farmacol, Fac Med Ribeirao Preto, Av Bandeirantes 3900, Ribeirao Preto, SP - Brazil
[3] Univ Estadual Londrina, Dept Enfermagem, Ctr Ciencias Saude, Av Robert Koch 60, Londrina, PR - Brazil
[4] Univ Estadual Londrina, Dept Ciencias Farmaceut, Ctr Ciencias Saude, Av Robert Koch 60, Londrina, Parana - Brazil
Número total de Afiliações: 4
Tipo de documento: Artigo Científico
Fonte: Mediators of Inflammation; 2019.
Citações Web of Science: 0
Resumo

Clinically active drugs for the treatment of acute pain have their prescription limited due to the significant side effects they induce. An increase in reactive oxygen species (ROS) has been linked to several conditions, including inflammation and pain processing. Therefore, new or repurposed drugs with the ability of reducing ROS-triggered responses are promising candidates for analgesic drugs. Vinpocetine is a clinically used nootropic drug with antioxidant, anti-inflammatory, and analgesic properties. However, the effects of vinpocetine have not been investigated in a model with a direct relationship between ROS, inflammation, and pain. Based on that, we aimed to investigate the effects of vinpocetine in a model of superoxide anion-induced pain and inflammation using potassium superoxide (KO2) as a superoxide anion donor to trigger inflammation and pain. In the KO2 model, vinpocetine dose-dependently reduced pain-like behaviors (spontaneous pain and hyperalgesia), paw edema, and neutrophil and mononuclear cell recruitment to the paw skin (assessed by H\&E staining, fluorescence, and enzymatic assays) and to the peritoneal cavity. Vinpocetine also restored tissue endogenous antioxidant ability and Nrf2 and Ho-1 mRNA expression and reduced superoxide anion production and gp91(phox) mRNA expression. We also observed the inhibition of I kappa B alpha degradation by vinpocetine, which demonstrates a reduction in the activation of NF-kappa B explaining the diminished production of IL-33, IL-1 beta, and TNF-alpha. Collectively, our data show that vinpocetine alleviates pain and inflammation induced by KO2, which is a mouse model with a direct role of ROS in triggering pain and other inflammatory phenomena. Thus, the results suggest the repurposing of vinpocetine as an anti-inflammatory and analgesic drug. (AU)

Processo FAPESP: 13/08216-2 - CPDI - Centro de Pesquisa em Doenças Inflamatórias
Beneficiário:Fernando de Queiroz Cunha
Linha de fomento: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs
Processo FAPESP: 11/19670-0 - Mecanismos envolvidos na fisiopatologia da artrite reumatóide, dor e sepse
Beneficiário:Fernando de Queiroz Cunha
Linha de fomento: Auxílio à Pesquisa - Temático