Protection of vascular endothelium by aspirin in a murine model of chronic Chagas’ diseReport as inadecuate

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Chronic Chagas’ disease affects 10–30 % of patientsinfected with Trypanosoma cruzi, and it mainly manifestsas cardiomyopathy. Important pathophysiologicalmechanisms involved in the cardiac lesions include activationof the endothelium and induced microvascularalterations. These processes involve the production of endothelialadhesion molecules and thromboxane A2, which areinvolved in inflammatory cell recruitment and platelet aggregation,respectively. Cyclooxygenase inhibitors such asaspirin decrease thromboxane production and alter thecourse of Chagas’ disease, both in the acute and chronicphases. We studied the effects of the administration of lowand high doses of aspirin during the early phase of T. cruziinfection, following microvascular damage in the context ofa chronic murine model of Chagas’ disease. The effectsof both schedules were assessed at 24 and 90 dayspostinfection by evaluating parasitemia, mortality, and cardiachistopathological changes as well as the expressionof ICAM, VCAM, and E-selectin in cardiac tissue.Thromboxane A2, soluble ICAM, and E-selectin bloodlevels were also measured. While aspirin did not affectparasitemia or mortality in the infected mice, it decreasedboth cardiac inflammatory infiltrates and thromboxanelevels. Additionally, at 90 days postinfection, aspirin normalizedsICAM and sE-selectin levels. Considering theimproved endothelial function induced by aspirin, we proposethe possibility of including this drug in clinical therapyto treat chronic Chagas’ disease.Nota general

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Author: Molina Berríos, Alfredo; - Campos Estrada, Carolina; - Lapier, Michel; - Duaso, Juan; - Kemmerling Weis, Ulrique; - Galanti Garr



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