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Fenofibrate protects against acute myocardial I/R injury in rat by suppressing mitochondrial apoptosis as decreasing cleaved caspase-9 activation.

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  • معلومة اضافية
    • المصدر:
      Publisher: IOS Press Country of Publication: Netherlands NLM ID: 101256509 Publication Model: Print Cited Medium: Internet ISSN: 1875-8592 (Electronic) Linking ISSN: 15740153 NLM ISO Abbreviation: Cancer Biomark Subsets: MEDLINE
    • بيانات النشر:
      Original Publication: Amsterdam ; Washington, DC : IOS Press, c2005-
    • الموضوع:
      Caspase 9/*metabolism ; Fenofibrate/*pharmacology ; Mitochondria/*drug effects ; Myocardial Reperfusion Injury/*prevention & control; Animals ; Apoptosis/drug effects ; Hypolipidemic Agents/pharmacology ; Male ; Mitochondria/enzymology ; Myocardial Reperfusion Injury/enzymology ; Myocardial Reperfusion Injury/pathology ; Random Allocation ; Rats ; Rats, Wistar
    • نبذة مختصرة :
      Background and Aims: Peroxisome proliferator-activated receptor-α (PPAR-α) activation has been reported to reduce myocardial ischemia-reperfusion (I/R) injury by inhibiting cell apoptosis. However, the antiapoptotic mechanism of PPAR-α is still unknown. Fenofibrate is a PPAR-α agonist In the present study, we investigate the effects and relevant mechanism of fenofibrate on experimental myocardial ischemia-reperfusion (I/R) injury in rats.
      Methods: Adult male Wistar rats were pretreated with fenofibrate (80 mg/kg) daily for a period of 7 days. After the treatment period, myocardial I/R injury model was made by left anterior descending coronary artery ligation for 45 min and reperfusion for 120 min. Myocardial infarct size, malondialdehyde (MDA) cleaved-caspase-9 protein expression, PPARα and uncoupling protein 2 (UCP2) mRNA levels in myocardial tissue were detected Cell apoptosis was detected by Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL). Serum lactate dehydrogenase and creatine kinase activities were measured in rats pretreated with fenofibrate The ultrastructure of myocardial tissues was observed.
      Results: Significant increases in myocardial cell apoptosis, malondialdehyde (MDA) level and cleaved-caspase-9 protein expression level in myocardial tissue were observed, along with reductions of PPARα and uncoupling protein 2 (UCP2) mRNA levels in myocardial tissue of the experimental myocardial ischemia-reperfusion (I/R) injury in rats. Impaired mitochondria were also observed under electron microscopic. However, pretreatment of ischemia/reperfusion rats with fenofibrate brought the biochemical parameters and related genes expression levels to near normalcy, indicating the protective effect of fenofibrate against myocardial ischemia/reperfusion injury in rats.
      Conclusions: The PPAR-α activator fenofibrate conferred cytoprotective effect against myocardial ischemia-reperfusion (I/R) injury in rats. Associated mechanisms involved decreased cleaved-caspase-9 expression and decreased cell apoptosis.
    • Contributed Indexing:
      Keywords: Acute myocardial ischemia/reperfusion injury; PPARα; apoptosis; caspase-9
    • الرقم المعرف:
      0 (Hypolipidemic Agents)
      EC 3.4.22.- (Casp9 protein, rat)
      EC 3.4.22.- (Caspase 9)
      U202363UOS (Fenofibrate)
    • الموضوع:
      Date Created: 20170607 Date Completed: 20180503 Latest Revision: 20180503
    • الموضوع:
      20240829
    • الرقم المعرف:
      10.3233/CBM-170572
    • الرقم المعرف:
      28582851