Chagas disease is a parasitic disease caused by Trypanosoma cruzi it is endemic in Latin America, where is a major health problem since it affects 8–10 million people, causes 50,000 deaths per year and about 25% of the population is at risk of acquiring the disease. It remains practically incurable, mainly because of the limited interest in developing new drugs and because the drugs available for its treatment, Benznidazole (Bz) and Nifurtimox (Nx) are inefficient to cure patients. The acute phase of the disease appears shortly after infection, the chronic phase appears after a silent asymptomatic period that may last several years. During the chronic phase, the heart, esophagus, colon and PNS are irreversibly affected, patients usually die from heart failure. The chronic phase may be established by the evasion of the immune response by the parasite, secondly because Bz and Nx generate free radicals that can affect the cells of the immune system (CIS) which could favour the chronic phase. In our research group, we design and synthesized the benzyl ester of Npropyl oxamic (NPOxB) that is an effective inhibitor of the alpha-hydroxy acid dehydrogenase II enzyme, which is a specific enzyme in the glycolytic pathway of the parasite. In this work we treated with NPOxB or Bz infected mice with NINOA or INC5 strains, we evaluate the parasitaemia, the macrophages, B, T, plasma and dendritic cells. The NPOx-B decreased more the parasitaemia of both T. cruzi strains than the Bz. The mice infected and treated with Bz showed a decrease in B, T and plasma cells compared to the infected mice treated with NPOxB. So NPOxB is more effective in decrease the parasitaemia and lacks the toxicity of Bz, it doesn’t affect in CIS, the cure of the disease can be achieved more efficiently.
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