Notch receptor expression in Trypanosoma cruzi infected Human Umbilical Vein Endothelial Cells treated with benznidazole or aspirin as revealed by microarray analysis

Chagas disease is a parasitic infection originally endemic to latinamerican countries but now spreaded worldwide that can be transmitted congenitally. Current specific therapy involves benznidazole, however, other therapies may modify gene expression that can change genetic expression profile, allowing cell programming to provide a more unfavorable environment for intracellular parasite development. Herein, microarray analysis was performed to Human Umbilical Vein Endothelial Cells (HUVEC), treated with benznidazole and the anti-inflammatory drugs aspirin or simvastatin, and infected with T. cruzi, the causative agent of Chagas disease. Human umbilical vein endothelial cells incubated for 24 hrs with Benznidazole (Bz) 20 µM, simvastatin (Simv) 5 µM, Aspirin (Asa) 125 uM, or Bz 10µM/Simv 1. After that, cells were challenged with Tryoanosoma cruzi trypomastigotes in cell:parasite ratio of 1:10. Total RNA was extarcted and microaray analysis was performed against SurePrint G3 Human GE 8x60K chips. Cells without parasites or pharmacological treatment were used as uninfected control.