Oleuropein Offers Cardioprotection in Rats with Acute Myocardial Infarction

Myocardial infarction causes a cascade of events, which leads to heart failure, debilitation and death. This study examined possible cardioprotective effect of oleuropein in rats with acute myocardial infarction. Male Sprague-Dawly rats were allocated to five groups: sham, myocardial infarction rece...

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Veröffentlicht in:Cardiovascular toxicology 2015-01, Vol.15 (1), p.61-68
Hauptverfasser: Janahmadi, Zeinab, Nekooeian, Ali Akbar, Moaref, Ali Reza, Emamghoreishi, Masoomeh
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Sprache:eng
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Zusammenfassung:Myocardial infarction causes a cascade of events, which leads to heart failure, debilitation and death. This study examined possible cardioprotective effect of oleuropein in rats with acute myocardial infarction. Male Sprague-Dawly rats were allocated to five groups: sham, myocardial infarction receiving vehicle, and three myocardial infarction receiving oleuropein at 10, 20, and 30 mg/kg/day for 7 days, and underwent sham operation or coronary ligation. Twenty-four hours later, animals underwent echocardiographic and hemodynamic studies, and infarct areas, serum concentrations of oxidative stress and inflammatory markers were determined. Myocardial infarction group receiving vehicle had significantly lower left ventricular developed and systolic pressures, rate of rise/decrease of left ventricular pressure, stroke volume, ejection fraction and cardiac output, and serum superoxide dismutase and glutathione reductase than those of sham group. Pretreatment with oleuropein prevented the reduction of these variables. Moreover, the group had a significantly higher serum malondialdehyde, interleukin-1β, TNF-α, creatin kinase-MB, and troponin I, lactate dehydrogenase, and infarct area than those of sham group. Pretreatment with oleuropein prevented the increase of these variables. The findings indicate that coronary ligation results in acute myocardial infarction characterized by impaired cardiac function, and oleuropein pretreatment prevented cardiac impairment partly by reducing oxidative stress and release of proinflammatory cytokines.
ISSN:1530-7905
1559-0259
DOI:10.1007/s12012-014-9271-1