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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Vinpocetine reduces diclofenac-induced acute kidney injury through inhibition of oxidative stress, apoptosis, cytokine production, and NF-kappa B activation in mice

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Fattori, Victor ; Borghi, Sergio M. ; Guazelli, Carla F. S. ; Giroldo, Andressa C. ; Crespigio, Jefferson ; Bussmann, Allan J. C. ; Coelho-Silva, Leticia ; Ludwig, Natasha G. ; Mazzuco, Tania L. ; Casagrande, Rubia ; Verri, Jr., Waldiceu A.
Total Authors: 11
Document type: Journal article
Source: PHARMACOLOGICAL RESEARCH; v. 120, p. 10-22, JUN 2017.
Web of Science Citations: 18
Abstract

Acute kidney injury (AKI) represents a complex clinical condition associated with significant morbidity and mortality. Approximately, 19-33% AKI episodes in hospitalized patients are related to drug-induced nephrotoxicity. Although, considered safe, non-steroidal anti-inflammatory drugs such as diclofenac have received special attention in the past years due to the potential risk of renal damage. Vinpocetine is a nootropic drug known to have anti-inflammatory properties. In this study, we investigated the effect and mechanisms of vinpocetine in a model of diclofenac-induced AKI. We observed that diclofenac increased proteinuria and blood urea, creatinine, and oxidative stress levels 24h after its administration. In renal tissue, diclofenac also increased oxidative stress and induced morphological changes consistent with renal damage. Moreover, diclofenac induced kidney cells apoptosis, up-regulated proinflammatory cytokines, and induced the activation of NF-kappa B in renal tissue. On the other hand, vinpocetine reduced diclofenac-induced blood urea and creatinine. In the kidneys, vinpocetine inhibited diclofenac-induced oxidative stress, morphological changes, apoptosis, cytokine production, and NF-kappa B activation. To our knowledge, this is the first study demonstrating that diclofenac-induced AKI increases NF-kappa B activation, and that vinpocetine reduces the nephrotoxic effects of diclofenac. Therefore, vinpocetine is a promising molecule for the treatment of diclofenac-induced AKI. (C) 2017 Elsevier Ltd. All rights reserved. (AU)

FAPESP's process: 13/08216-2 - CRID - Center for Research in Inflammatory Diseases
Grantee:Fernando de Queiroz Cunha
Support Opportunities: Research Grants - Research, Innovation and Dissemination Centers - RIDC