Trypanosoma cruzi against

Bfx and Fx derivatives have been evaluated against the parasites Trypanosoma cruzi (T. cruzi), which is responsible for American Trypanosomiasis and Plasmodium falciparum (P. falciparum) responsible for Malaria. 

Pathophysiology can influence muscarinic activity in other ways as well. Circulating autoantibodies against the second extracellular loop of cardiac M2 muscarinic receptors have been detected in some patients with idiopathic dilated cardiomyopathy and those afflicted with Chagas1 disease caused by the protozoan Trypanosoma cruzi. These antibodies exert parasympathomimetic actions on the heart that are prevented by atropine. In animals immunized with a peptide from the second extracellular loop of the M2 receptor, the antibody is an allosteric modulator of the receptor. Although their role in the pathology of heart failure is unknown, these antibodies should provide clues to the molecular basis of receptor activation because their site of action differs from the orthosteric site where acetylcholine binds (see Chapter 2). 

JA13474>. A trypanocidal phenazine derived from p-lapachone was found to be active against Trypanosoma cruzi, the microorganism that causes Chagas disease, and its structure was determined in part by X-ray crystallography <02JMC2112>. 

In a double-blind, randomized, clinical trial, benznidazole 5 mg/kg/day for 60 days was compared with placebo in children in the indeterminate phase of infection by Trypanosoma cruzi (1). In general, treatment was well tolerated. The treated children had a significant reduction in mean titers of antibodies against T. cruzi measured by indirect hemagglutination, indirect immunofluorescence, and ELISA. At 4-year follow-up, 62% of the benznidazole-treated children and no placebo-treated chUd were seronegative for T. cruzi. Xenodiagnosis after 48 months was positive in 4.7% of the benznidazole-treated children and in 51% of the placebo-treated children. 

Berberine chloride was tested for in vitro activity against the epimastigotes of the protozoan parasite Trypanosoma cruzi (Costa Rican strain). This organism is the causative agent of Chagas Disease. The alkaloid was found to inhibit the growth of the epimastigotes at concentrations of both 5 pg/ml and 50 pg/ml [224]. 

M. B. Reyes, M. Lorca, P. Munoz, and A. C. C. Frasch, Fetal IgG specificities against Trypanosoma cruzi antigens in infected newborns, Proc. Natl. Acad. Sci. USA, 87 (1990) 2846—2850. 

M. S. Leguizamon, O. E. Campetella, S. M. Gonzalez-Cappa, and A. C. C. Frasch, Mice infected with Trypanosoma cruzi produce antibodies against the enzymatic domain of trans-sialidase that inhibit its activity, Infect. Immun., 62 (1994) 3441—3446. 

Campnosperma panamense Standi, (leaves) Lanaroflavone (249). Antiprotozoal activity. antimalarial and leishmanicidal activities, but inactive against Chagas disease vector. Trypanosoma cruzi. Weniger et al., 2001 [126], 2004 [70], 2006[86]. 

Garcinia intermedia Pittier Hammei (leaves) Biflavones. Podocarpusflavone A (6) amentoflavone (1). Trypanocidal activity against epimastigotes of Trypanosoma cruzi, the etiologic agent of Chagas disease. Abe et al., 2004[170]. 

Cissampelos pareira L. (aerial parts) (I-P,0,II-7 I-a, II-6)-Chalcone-flavone Cissampeloflavone (311). Antiprotozoal activity, against Trypanosoma cruzi and T. brucei rhodiense, and has a low cytotoxicity in the human KB cell line. Ramirez et al., 2003 [247] Maya et al.,2007[248]. 

Maya, J. D. Cassels, B. K. Iturriaga-Vasquez, P. Ferreira, J. Faundez, M. Galanti, N. Ferreira, A. Morello, A., Mode of action of natural and synthetic drugs against Trypanosoma cruzi and their interaction with the mammalian host. Comp. Biochem. Physiol. - Part A Mol Integr. Physiol, 2007, 146, 601-620. 

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