Fig. 2.
Fenofibrate reverses cardiac functional failure in mice infected with Trypanosoma cruzi. BALB/c mice were infected by intraperitoneal route with 1 x 105 bloodstream trypomastigotes of the non-lethal K-98 clone of T. cruzi for 6 weeks, followed by intraperitoneal re-infection with 100 bloodstream trypomastigotes of the lethal RA strain of T. cruzi for 4 weeks. PPAR-α mRNA levels and PPAR-α expression were determined by RT-qPCR and Western blot with specific primers and antibodies, respectively. The RT-qPCR results were normalized against 18S rRNA. Protein levels were normalized against α-actin (A). Infected mice were treated with different doses of Fenofibrate (Fen). Ejection fraction and Shortening fraction were evaluated by echocardiography (B). Infected mice were treated with 25 mg/kg/day Bzl for 15 consecutive days. At the same time treatment with 100 mg/kg/day Fen was initiated and continued for 30 consecutive days. The ejection fraction, shortening fraction, left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD) and isovolumic relaxation time (IVRT) were evaluated by echocardiography (C). Parasitaemia (parasites/mL x 103) and heart parasite load were analysed in infected or infected-treated mice (D). Results are expressed as the mean of three independent experiments (seven mice/group) ± SEM. White bar: Uninfected control mice. Black bar: T. cruzi-infected mice. Hatched white bar: T. cruzi and Bzl treated mice. Grey bar: T. cruzi and Fen treated mice. Hatched grey bar: T. cruzi and Fen-Bzl treated mice. **P < 0.001, ***P < 0.0001, T. cruzi-infected and treated mice (Fen or Fen plus Bzl) vs. T. cruzi-infected mice; ##P < 0.001, ###P < 0.0001, T. cruzi-infected mice vs. uninfected mice.