Jan 17, 2009

Effect of allopurinol on cardiomyocyte apoptosis in rats after myocardial infarction

European Journal of Heart Failure
Jun XiaoKaishun Huang


This study was designed to explore the effect of the xanthine oxidase (XO) inhibitor allopurinol on cardiomyocyte apoptosis after myocardial infarction (MI) in a rat model. MI was induced in rats by ligation of the anterior descending coronary artery. Survivors were randomly divided into three groups: sham operation group, MI group, and allopurinol group (50 mg kg(-1) day(-1)). After 28 days, infarction size was measured. In non-infarcted zones (NIZ), apoptosis index (AI) was measured by TUNEL [terminal deoxynucleotidyl transferase (TdT)-mediated digoxigenin-conjugated dUTP nick-end labelling]; expression of Fas was detected by immunohistochemistry, and expression of XO and Caspase-3 by western blot. In addition, XO and O(2)(-), OH-scavenging activity of myocardial tissue in the NIZ were measured by colorimetry. Results suggest that AI and expression of Fas and Caspase-3 in the NIZ were significantly depressed in the allopurinol group, compared with MI group; moreover, activity of XO was significantly decreased while O(2)(-) and OH-scavenging activity were significantly increased in the allopurinol group. Ventricular remodelling was attenuated but there were no significant differences in infarct size or XO expression levels bet...Continue Reading

Mentioned in this Paper

Salicylhydroxamic acid
Apoptosis, Intrinsic Pathway
Depressed - Symptom
Western Blotting
Oxidative Stress
Myocardial Infarction

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Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis