<h5>Introduction</h5> Chagas' disease, caused by Trypanosoma cruzi infection, is one of the main causes of death due to heart failure in Latin American countries. About one fourth of infected individuals develop chronic cardiomyopathy, the most severe form of the disease. The unique treatment available for patients with severe heart failure is heart transplantation. Stem cell-based therapy is currently being investigated as a treatment for heart failure, including for Chagas' disease. An alternative to stem cell transplantation is the use of growth factors to mobilize bone marrow cells to the periphery. In this work, we investigated the effects of G-CSF administration in our experimental model of chronic chagasic cardiomyopathy.</P><h5>Methods</h5> We used a well-established model of chronic chagasic cardiomyopathy in C57Bl/6 mice inoculated with 1000 trypomastigotes of the Colombian strain of T. cruzi . Three different experimental groups were analyzed. The first one without treatment, the second treated with human recombinant G-CSF administered in a dose of 200 μg/kg per day during 5 consecutive days (one cycle of treatment) and the third one treated with three cycles of G-CSF administration. We started functional and histopathological analysis 2 months after the end of treatment. We performed functional analysis by ECG recording in all experimental groups with animals under anesthesia (xilasine and ketamine). Data were stored for analysis using Chart 5 software for evaluation of physiological parameters. Histopathological evaluation was done by morphometry studies in order to quantify the number of inflammatory cells by light microscopy in sections stained with standard hematoxylin and eosin. The fibrotic area was evaluated after Sirius red staining. Morphometric analyses were carried out using the Image Pro Program to integrate the areas of fibrotic and nonfibrotic tissue in each field.</P><h5>Results</h5> In the group treated with three cycles of G-CSF, the reduction in fibrotic area was 73% and the number of inflammatory cells was diminished in 38% compared to control mice. In the group treated with one cycle of G-CSF administration, a discrete reduction in fibrosis (13%) was found, but no alteration in the degree of inflammation was observed. All chronic chagasic mice had cardiac electrical disturbances that included atrioventricular blockage, intraventricular conduction disturbances and abnormal cardiac rhythm before treatment. The functional analysis by ECG did not reveal any improvement in cardiac electrogenesis 2 months after treatment.</P><h5>Conclusion</h5> Treatment with G-CSF decreases inflammation and fibrosis in chronic chagasic mice. This effect, however, did not reflect a reversion of cardiac electrical disturbances characteristic of chronic chagasic cardiomyopathy.</P>
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Treatment with granulocyte colony stimulating factor in a mouse model of chronic chagasic cardiomyopathy
Dos Santos, R.; Macambira, S.G.; Lima, R.S.; Senra, J.F.; Costa, C.; Guimaraes, P.; Soares, M.
Follow Cardiovascular Revascularization Medicine
, Volume 8 (2)
Elsevier – Apr 1, 2007
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