Open AccessACE2 activator diminazene aceturate exerts renoprotective effects in gentamicin-induced acute renal injury in rats
Author(s) -
Tatiane Cristine Silva de Almeida,
Katharina Lanza,
Roberta da Silva Filha,
Leda Maria de Castro C. Campos,
Esdras Guedes Fonseca,
Mariana W. Chagas,
Natália Pessoa Rocha,
Marcos Augusto de Sá,
Maria Aparecida Ribeiro Vieira,
Marcelo Vidigal Caliari,
Lucas M. Kangussu,
Anderson J. Ferreira,
Ana Cristina Simões e Silva
Publication year - 2020
Publication title -
clinical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.91
H-Index - 138
eISSN - 1470-8736
pISSN - 0143-5221
DOI - 10.1042/cs20201022
Subject(s) - pharmacology , medicine , renin–angiotensin system , renal function , kidney , activator (genetics) , diminazene , acute kidney injury , angiotensin ii , angiotensin converting enzyme 2 , disease , immunology , blood pressure , receptor , infectious disease (medical specialty) , covid-19 , trypanosomiasis
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.