ACE2 activator diminazene aceturate exerts renoprotective effects in gentamicin-induced acute renal injury in rats
| Autor: | Natalia Pessoa Rocha, Katharina Lanza, Marcelo Vidigal Caliari, Esdras Guedes Fonseca, Roberta da Silva Filha, Tatiane Cristine Silva de Almeida, Lucas M. Kangussu, Anderson J. Ferreira, Marcos Augusto de Sá, Mariana W. Chagas, Leda Maria de Castro C. Campos, Maria Aparecida Ribeiro Vieira, Ana Cristina Simões e Silva |
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| Rok vydání: | 2020 |
| Předmět: |
Male
Enzyme Activators Renal function Pharmacology Kidney Protective Agents urologic and male genital diseases Renin-Angiotensin System Renin–angiotensin system medicine Animals Rats Wistar Inflammation Activator (genetics) business.industry Body Weight Therapeutic effect Acute kidney injury General Medicine Acute Kidney Injury medicine.disease Angiotensin II Angiotensin-converting enzyme 2 Cytokines Gentamicin Angiotensin-Converting Enzyme 2 Gentamicins business Diminazene Biomarkers hormones hormone substitutes and hormone antagonists medicine.drug |
| Zdroj: | Clinical Science. 134:3093-3106 |
| ISSN: | 1470-8736 0143-5221 |
| DOI: | 10.1042/cs20201022 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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