Repurposing of the Nootropic Drug Vinpocetine as an Analgesic and Anti-Inflammatory Agent: Evidence in a Mouse Model of Superoxide Anion-Triggered Inflammation
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...
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Published in | Mediators of inflammation Vol. 2019; no. 2019; pp. 1 - 14 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Cairo, Egypt
Hindawi Publishing Corporation
01.01.2019
Hindawi John Wiley & Sons, Inc Hindawi Limited |
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Online Access | Get full text |
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Abstract | 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 gp91phox mRNA expression. We also observed the inhibition of IκBα degradation by vinpocetine, which demonstrates a reduction in the activation of NF-κB explaining the diminished production of IL-33, IL-1β, and TNF-α. 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. |
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AbstractList | 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 gp91phox mRNA expression. We also observed the inhibition of IκBα degradation by vinpocetine, which demonstrates a reduction in the activation of NF-κB explaining the diminished production of IL-33, IL-1β, and TNF-α. 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. 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 (K[O.sub.2]) as a superoxide anion donor to trigger inflammation and pain. In the K[O.sub.2] 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.sup.phox] mRNA expression. We also observed the inhibition of I[kappa]Ba 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 K[O.sub.2], 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. 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 (KO 2 ) as a superoxide anion donor to trigger inflammation and pain. In the KO 2 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 κ B α degradation by vinpocetine, which demonstrates a reduction in the activation of NF- κ B explaining the diminished production of IL-33, IL-1 β , and TNF- α . Collectively, our data show that vinpocetine alleviates pain and inflammation induced by KO 2 , 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. 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 (KO ) as a superoxide anion donor to trigger inflammation and pain. In the KO 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 and mRNA expression and reduced superoxide anion production and mRNA expression. We also observed the inhibition of I B degradation by vinpocetine, which demonstrates a reduction in the activation of NF- B explaining the diminished production of IL-33, IL-1 , and TNF- . Collectively, our data show that vinpocetine alleviates pain and inflammation induced by KO , 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. |
Audience | Academic |
Author | Lourenco-Gonzalez, Yuri Bernardy, Catia C. F. Verri, Waldiceu A. Domiciano, Talita P. Borghi, Sergio M. Alves-Filho, José C. Cunha, Thiago Mattar Zaninelli, Tiago H. Casagrande, Rúbia Cunha, Fernando Queiroz Rossaneis, Ana C. Fattori, Victor |
AuthorAffiliation | 1 Departamento de Ciências Patológicas, Centro de Ciências Biológicas, Universidade Estadual de Londrina, Rod. Celso Garcia Cid km 480 PR 445, Londrina, Paraná, Brazil 2 Departamento de Farmacologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Av. Bandeirantes 3900, Ribeirão Preto, São Paulo, Brazil 4 Departamento de Ciências Farmacêuticas, Centro de Ciências da Saúde, Universidade Estadual de Londrina, Av. Robert Koch 60, Londrina, Paraná, Brazil 3 Departmento de Enfermagem, Centro de Ciências da Saúde, Universidade Estadual de Londrina, Av. Robert Koch 60, Londrina, PR, Brazil |
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Author_xml | – sequence: 1 fullname: Cunha, Fernando Queiroz – sequence: 2 fullname: Casagrande, Rúbia – sequence: 3 fullname: Verri, Waldiceu A. – sequence: 4 fullname: Alves-Filho, José C. – sequence: 5 fullname: Bernardy, Catia C. F. – sequence: 6 fullname: Zaninelli, Tiago H. – sequence: 7 fullname: Borghi, Sergio M. – sequence: 8 fullname: Rossaneis, Ana C. – sequence: 9 fullname: Domiciano, Talita P. – sequence: 10 fullname: Fattori, Victor – sequence: 11 fullname: Lourenco-Gonzalez, Yuri – sequence: 12 fullname: Cunha, Thiago Mattar |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31049025$$D View this record in MEDLINE/PubMed |
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ContentType | Journal Article |
Copyright | Copyright © 2019 Yuri Lourenco-Gonzalez et al. COPYRIGHT 2019 John Wiley & Sons, Inc. Copyright © 2019 Yuri Lourenco-Gonzalez et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0 Copyright © 2019 Yuri Lourenco-Gonzalez et al. 2019 |
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SubjectTerms | Abdomen Analgesics Analysis Anti-inflammatory drugs Antioxidants Arthritis Care and treatment Central nervous system agents Cognitive enhancement Disease Drug development Drug dosages Edema Experiments Gene expression Hyperalgesia IL-1β Immunology Inflammation Kidneys Neurons Neutrophils NF-κB protein Nonsteroidal anti-inflammatory drugs Oxidation Pain Pain perception Peritoneum Potassium Reactive oxygen species Scientific equipment and supplies industry Skin Superoxide Tumor necrosis factor-α Vinpocetine |
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Title | 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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