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Enalapril e captopril revertem o edema e a hiperplasia renais causados pelo antimoniato de N-metilglucamina em camundongos C57BL/6

Por: Tipo de material: ArtigoArtigoAssunto(s): Recursos online: Em: Arquivo Brasileiro de Medicina Veterinária e Zootecnia (Brazil) v. 68(4) p. 1095-1098; (2016)Sumário: 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 Nmethylglucamine 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. Keywords: enzyme-converting inhibitors, glucantime, renototoxicidade
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Periódicos Periódicos Biblioteca Nacional de Agricultura - Binagri Periódicos agrícolas 2016 v. 68(4) Texto integral (PDF) Consulta local 2025-0570


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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 Nmethylglucamine 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.


Keywords: enzyme-converting inhibitors, glucantime, renototoxicidade

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