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

2020; Portland Press; Volume: 134; Issue: 23 Linguagem: Inglês

10.1042/cs20201022

1470-8736

Tatiane Cristine Silva de Almeida, Katharina Lanza, Roberta da Silva Filha, Leda M. C. Coimbra-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,

Acute Kidney Injury Research

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.