Benznidazole prevents endothelial damage in an experimental model of Chagas disease

Molina-Berrios, A; Campos Estrada C; Lapier, M.; Duaso, J.; Kemmerling U.; Galanti N.; Leiva, M; Ferreira J.; Lopez-Munoz, R; Maya, JD

Abstract

Objectives: To evaluate the effect of benznidazole on endothelial activation in a murine model of Chagas disease. Methods: A low (30 mg/kg/day) and a high (100 mg/kg/day) dose of benznidazole were administered to mice infected with Trypanosoma cruzi during the early phases of the infection. The effects of the treatments were assessed at 24 and 90 days postinfection by evaluating the parasitaemia, mortality, histopathological changes and expression of ICAM in the cardiac tissue. The blood levels of thromboxane A(2), soluble ICAM and E-selectin were also measured. T. cruzi clearance was assessed by the detection of parasite DNA in the heart tissue of infected mice. Results: Benznidazole decreased the cardiac damage induced by the parasite, and amastigote nests disappeared at 90 days postinfection. Both doses cleared the parasite from the cardiac tissue at 24 and 90 days postinfection. In addition, benznidazole decreased the thromboxane levels and normalized the plasma sICAM and sE-selectin levels by 90 days postinfection. Conclusions: Early administration of benznidazole at a dose as low as 30 mg/kg eradicates T. cruzi from cardiac tissue. Additionally, benznidazole prevents cardiac damage and modulates endothelial activation as part of its antichagasic activity. (C) 2013 Elsevier B.V. All rights reserved.

Más información

Título según WOS: Benznidazole prevents endothelial damage in an experimental model of Chagas disease
Título según SCOPUS: Benznidazole prevents endothelial damage in an experimental model of Chagas disease
Título de la Revista: ACTA TROPICA
Volumen: 127
Número: 1
Editorial: ELSEVIER SCIENCE BV
Fecha de publicación: 2013
Página de inicio: 6
Página final: 13
Idioma: English
URL: http://linkinghub.elsevier.com/retrieve/pii/S0001706X13000740
DOI:

10.1016/j.actatropica.2013.03.006

Notas: ISI, SCOPUS