International Journal of Molecular Sciences · 9 authors, 6 centres
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In a rat model of metabolic syndrome, pre-treatment with the PPARα agonist clofibrate before cardiac ischemia/reperfusion injury reduced inflammation, fibrosis, and apoptosis. This was associated with a decrease in the compensatory expression of atrial natriuretic peptide and its receptor.
This preclinical study used a rat model of metabolic syndrome (MetS) to investigate the effects of a 7-day pre-treatment with clofibrate on cardiac ischemia/reperfusion (I/R) injury. The central result was that clofibrate significantly decreased the inflammatory response, as evidenced by reduced levels of IL-1β, IL-6, and TNF-α in left ventricles. This reduction in inflammation led to decreases in myocardial fibrosis, the expression of matrix metalloprotease 2, and cardiomyocyte apoptosis. The study also found that elevated atrial natriuretic peptide (ANP) and its receptor (ANPr) expression in MetS hearts, particularly after I/R, was a compensatory response that was diminished by clofibrate treatment. Limitations include the use of a specific animal model, with findings having only indirect human relevance, and the study did not evaluate specific inflammatory cell subpopulations.
