Benznidazole prevents endothelial damage in an experimental model of chagas disease
Autor: | Carolina Campos-Estrada, Mario Leiva, Michel Lapier, Alfredo Molina-Berríos, Juan Duaso, Ulrike Kemmerling, Juan Diego Maya, Rodrigo López-Muñoz, Jorge Ferreira, Norbel Galanti |
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Jazyk: | angličtina |
Rok vydání: | 2013 |
Předmět: |
Male
Chagas disease Thromboxane Trypanosoma cruzi Veterinary (miscellaneous) Endothelial activation Mice parasitic diseases medicine Animals Parasite hosting Chagas Disease Amastigote Trypanocidal agent Mice Inbred BALB C Dose-Response Relationship Drug biology biology.organism_classification medicine.disease Trypanocidal Agents Infectious Diseases Nitroimidazoles Benznidazole Insect Science Immunology Parasitology Endothelium Vascular medicine.drug |
Zdroj: | ACTA TROPICA Artículos CONICYT CONICYT Chile instacron:CONICYT |
Popis: | 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. |
Databáze: | OpenAIRE |
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