Effect of Colchicine on Myocardial Injury Induced by Trypanosoma cruzi in Experimental Chagas Disease

Colchicine treatment reversibly blocks cytokinesis but not mitosis in Trypanosoma cruzi epimastigotes

“…Colchicine is also used as a second-line treatment for cardiovascular diseases (Norrid and Oliphant 2014), and research is currently focused on colchicine analogs for potential use as antitumor therapy (Larocque et al 2014;Satpati et al 2014). The effect of colchicine has been studied on myocardial injury induced by T. cruzi in experimental Chagas' disease in hamsters (Fernandes et al 2012), in in vitro cultured cells (Rosestolato et al 2002;Tyler et al 2005), and in in vitro cultured parasites (Filho et al 1978). To better understand the action of colchicine over T. cruzi microtubules, here we performed experiments incubating epimastigote cultures in the presence of the drug, with the subsequent analysis of parasite morphology and DNA content using flow cytometry and immunofluorescence microscopy.…”

Introducing variability in targeting the microtubules: Review of current mechanisms and future directions in colchicine therapy

“…71 Colchicine decreased fibrosis and enhanced activity of matrix metalloproteinase-2 in hamsters with experimental Chagas disease. 72 Colchicine administration in the unilateral ureteral obstruction model results in suppressed interstitial fibrosis, decreased fibrogenic gene expression, and reduction in the levels of caspase-3, fibronectin, and ED-1. 73,74 The upregulation of profibrotic cytokine connective tissue growth factor (CTGF) by mechanical strain is dependent on RhoA activation.…”

Colchicine as an anti-inflammatory and cardioprotective agent

“…The drug also increased levels of matrix metalloproteinase-2 and dampened interstitial myocardial fibrosis in experimental myocarditis [22]. Antifibrotic effects of colchicine were also evident in experimental right ventricular damage and pulmonary arterial hypertension, where activity of matrix metalloproteinase-9, tissue growth factor-b, nuclear factor kB and other inflammatory agents was modulated in response to the therapy [23].…”