Indian Journal of Pharmacology · 2014 · 13 citations · 2 references
MedicineCardiologyPharmacologyApoptosisInflammationRedox BiochemistryCardiac BiomarkersIschemic Heart DiseaseMyocardial ProtectionCardioprotective TherapyIschemia-reperfusion Injury MonitoringMechanisms Of Cardiac InjuryMyocardial Injury DetectionMyocardial Ischemia MarkersMyocardial Ischemia-reperfusion InjuryOxidative Stress In Ischemia-reperfusion InjuryTerminal Deoxynucleotidyl Transferase Dutp Nick End Labeling
OBJECTIVES: To evaluate the cardioprotective effects of trapidil on myocardial ischemia-reperfusion injury (MIRI) in rabbits. MATERIALS AND METHODS: Rabbits were subjected to 40 min of myocardial ischemia followed by 120 min of reperfusion. Blood for superoxide dismutase (SOD) and malondialdehyde (MDA) were estimated. At the end of reperfusion, the rabbits were sacrificed and the hearts were isolated for histological examination. An apoptotic index (AI) was determined using the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end-labeling (TUNEL) method. The expression of apoptosis-related proteins Bax and Bcl-2 was analyzed using immunohistochemistry. Statistical analyses were performed by one-way analysis of variance (ANOVA), P < 0.05 considered statistically significant. RESULTS: Trapidil caused a significant (P < 0.05) increase in SOD activity, as decreased MDA levels and significantly (P < 0.05) reduced the expression of Bax as compared with the ischemia-reperfusion (IR) control group. CONCLUSION: Trapidil may attenuate the myocardial damage produced by IR injury and offer potential cardioprotective action.
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