Considerations on the mechanisms involved on the benefits of GM1 treatment of mice with experimental Chagas´ disease

Sadí Cossy Isasi, Juan Carlos Muiño

Abstract


Background: In previous papers, some of us reported that GM1 improve the condition of with acute Trypanosoma cruzi infection but the mechanisms proposed did not involve adrenergic or steroid receptors.

 

Methods: 160 three months old outbreed Albino Swiss mice were divided in four groups: a) non-infected, b) non-infected and treated with GM1 0,1 mg /day by intramuscular injection, for 30 days, c) infected with T. cruzi, 0.7´105 parasites, d) infected with T. cruzi, 0.7´105 parasites and treated with GM1 0,1 mg /day by intramuscular injection for 30 days. The animals were studied at 35 days from the beginning of treatment and at 120 days post treatment. Cardiomyocyte membranes were isolated and β adrenergic receptors, membrane fluidity and composition, plasma glucose, potassium, DHA, estradiol and cortisol were determined. Histological sections of heart and adrenal glands were examined.

 

Results:  At day 35 receptor Kd (nM) was 3.6; 4.46; 1.89 for healthy, infected, and infected GM1 treated mice and Bmax (fmol/mg prot) was 71.9; 54.8 and 21.14 respectively. At 120 days Kd for each group was 4.6; 4.6; and 2.79 respectively and Bmax was 71.9; 54.89; 74.2 respectively. Fluorescence anisotropy was reduced by infection and GM1 treatment from 0.88; 0.56; 0.43 for healthy, infected, and infected GM1 treated mice.  

GM1 treatment increased plasma estradiol in both sexes uninfected mice. Chronically infected mice with prolonged QT 59.5 ms presented 48.9 ms after GM1. Histology of cardiac muscle slices showed no fibrosis and adrenal glands remodeling.

 

Conclusions: GM1 improved the condition of acute lethal infected and chronically infected mice regulating beta adrenergic receptors directly or through the modulation of steroids hormones. The observed evolution was concomitant with structural tissue modifications.


Keywords


Experimental Chagas Disease; GM1; receptors; adrenal glands

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References


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DOI: http://dx.doi.org/10.18103/imr.v3i7.523

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