ACE2 activator diminazene aceturate exerts renoprotective effects in gentamicin-induced acute renal injury in rats

Author:

Silva de Almeida Tatiane Cristine12,Lanza Katharina3,da Silva Filha Roberta3,C. Campos Leda Maria de Castro4ORCID,Fonseca Esdras G.4,Chagas Mariana W.4,Rocha Natalia Pessoa3,de Sá Marcos Augusto2,Vieira Maria Aparecida Ribeiro4,Caliari Marcelo Vidigal5,Kangussu Lucas M.2,Ferreira Anderson José2,Simões e Silva Ana Cristina3

Affiliation:

1. Nuclear Technology Development Center (CDTN), Biological Science Institute – Federal University of Minas Gerais, Belo Horizonte, MG, Brazil

2. Department of Morphology, Biological Science Institute – Federal University of Minas Gerais, Belo Horizonte, MG, Brazil

3. Interdisciplinary Laboratory of Medical Investigation, Biological Science Institute – Faculty of Medicine, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil

4. Department of Physiology and Biophysics, Biological Science Institute – Federal University of Minas Gerais, Belo Horizonte, MG, Brazil

5. Department of General Pathology, Biological Science Institute – Federal University of Minas Gerais, Belo Horizonte, MG, Brazil

Abstract

Abstract Acute Kidney Injury (AKI) comprises a rapidly developed renal failure and is associated with high mortality rates. The Renin–Angiotensin System (RAS) plays a pivotal role in AKI, as the over-active RAS axis exerts major deleterious effects in disease progression. In this sense, the conversion of Angiotensin II (Ang II) into Angiotensin-(1-7) (Ang-(1-7)) by the Angiotensin-converting enzyme 2 (ACE2) is of utmost importance to prevent worse clinical outcomes. Previous studies reported the beneficial effects of oral diminazene aceturate (DIZE) administration, an ACE2 activator, in renal diseases models. In the present study, we aimed to evaluate the therapeutic effects of DIZE administration in experimental AKI induced by gentamicin (GM) in rats. Our findings showed that treatment with DIZE improved renal function and tissue damage by increasing Ang-(1-7) and ACE2 activity, and reducing TNF-α. These results corroborate with a raising potential of ACE2 activation as a strategy for treating AKI.

Publisher

Portland Press Ltd.

Subject

General Medicine

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