Registro completo |
Provedor de dados: |
Arq. Bras. Med. Vet. Zootec.
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País: |
Brazil
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Título: |
Enalapril e captopril revertem o edema e a hiperplasia renais causados pelo antimoniato de N-metilglucamina em camundongos C57BL/6
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Autores: |
Oliveira,S.S.
Lopes,L.L.
Damazo,A.S.
Albuquerque,D.
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Data: |
2016-08-01
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Ano: |
2016
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Palavras-chave: |
Inibidores da enzima conversora de angiotensina
Glucantime
Renototoxicidade
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Resumo: |
ABSTRACT The aim of this study was to verify whether enalapril and captopril would reverse the renal damage caused by N-methylglucamine antimoniate in C57BL/6 mice. We used inbred C57BL/6 female mice, obtained from the Oswaldo Cruz Foundation (FIOCRUZ), Salvador, BA. The mice were divided into four groups as follows: Group1: received saline by the intramuscular (IM) route; Group 2: received N-methylglucamine antimonate (IM); Group 3: received N-methylglucamine antimoniate and captopril; Group 4: was treated with N-methylglucamine antimoniate and enalapril. Both enalapril and captopril were orally administered in drinking water (ad libitum). After 30 days of treatment, the animals were sacrificed and their kidneys were collected for histological analysis which showed that enalapril completely reversed the edema, the podocytes hyperplasia and nucleus of the epithelial cells in the proximal convoluted tubules caused by N-methylglucamine antimoniate. On the other hand, the captopril treatment partially inhibited kidney harmful effects caused by N-metilgucamina antimoniate. Taken together, we would conclude that enalapril and captopril reverse edema and renalhyperplasia caused by N-methylglucamine antimonate in mice.
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Tipo: |
Info:eu-repo/semantics/other
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Idioma: |
Português
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Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0102-09352016000401095
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Editor: |
Universidade Federal de Minas Gerais, Escola de Veterinária
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Relação: |
10.1590/1678-4162-8925
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Formato: |
text/html
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Fonte: |
Arquivo Brasileiro de Medicina Veterinária e Zootecnia v.68 n.4 2016
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Direitos: |
info:eu-repo/semantics/openAccess
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