

Author: Ravingerová Táňa Adameová Adriana Kelly Tara Antonopoulou Efthymia Pancza Dezider Ondrejčáková Mária Khandelwal Vinoth K. M. Čarnická Slávka Lazou Antigone
Publisher: NRC Research Press
ISSN: 1205-7541
Source: Canadian Journal of Physiology and Pharmacology, Vol.87, Iss.12, 2009-12, pp. : 1028-1036
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Abstract
Peroxisome proliferator-activated receptors (PPAR), which are key transcriptional regulators of lipid metabolism and energy production, have been suggested to play an important role in myocardial ischaemia-reperfusion (I/R) injury. Their role in cardioprotection, however, is not yet fully elucidated. Statins have shown beneficial effects on I/R damage beyond lipid lowering, and some of their cardioprotective cholesterol-independent effects may be related to the regulation of PPAR. To clarify this issue, we explored a potential link between a response to I/R and changes in cardiac PPARα protein and gene expression in simvastatin-treated normocholesterolaemic rats. After 5 days of treatment with simvastatin (10 mg/kg per day, p.o.), Langendorff-perfused hearts were subjected to 30 min regional ischaemia (occlusion of the left anterior descending coronary artery) or global ischaemia and 2 h reperfusion for the evaluation of the infarct size (triphenyltetrazolium chloride and planimetry; as percentage of risk area), ischaemic arrhythmias, and postischaemic contractile recovery. Baseline PPARα mRNA and protein levels were increased by 3-fold and 2-fold, respectively, in simvastatin-treated hearts compared with the untreated controls. Simvastatin-treated hearts exhibited smaller size of infarction (11.5% ± 0.4% vs. 33.7% ± 4% in controls;
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