Key result
Pretreatment with 10 μg/kg luteolin significantly reduced myocardial infarct size from 18.6% to 10.0% of the area at risk and eliminated mortality during ischemia-reperfusion injury in rats.
Why the study?
Does luteolin reduce ischemia-reperfusion injury and arrhythmias in a rat model of myocardial ischemia?
Does luteolin reduce ischemia-reperfusion injury and arrhythmias in a rat model of myocardial ischemia?
Absolute Event Rate: 10% vs 18.6%
p-value: p=<0.05
Luteolin protects the myocardium against ischemia-reperfusion injury and arrhythmias in rats, likely through downregulation of NO production and antioxidant effects.
Luteolin may protect rat myocardium from ischemia-reperfusion injury; hypothesis-generating and should not change clinical practice.
BACKGROUND: Antioxidants effectively reduce ischemia-reperfusion (IR) injury. The cardioprotective effects of luteolin, a flavonoid that exhibits antioxidant properties and is widely available in many fruits and vegetables, were examined in rats subjected to myocardial IR injury. METHODS AND RESULTS: Rats were subjected to myocardial ischemia or reperfusion injury to evaluate the antiarrhythmic effects of luteolin. Myocardial infarct size was determined histochemically with triphenyltetrazolium chloride staining of the left ventricle. Luteolin was administered intravenously 15min before occlusion of the coronary artery. The incidence and duration of ventricular tachycardia and ventricular fibrillation and mortality during myocardial ischemia were significantly reduced by luteolin (10µg/kg). Similarly, luteolin (1µg/kg) reduced ventricular arrhythmias and mortality during the reperfusion phase. Pretreatment with luteolin decreased plasma lactate dehydrogenase and nitric oxide (NO) levels. Luteolin (10µg/kg) significantly reduced the myocardial infarct size, as well as malondialdehyde production in tissue samples of myocardial IR injury. Luteolin also downregulated inducible NO synthase protein and mRNA expression, but did not significantly alter neuronal NO synthase or endothelial NO synthase expression. CONCLUSIONS: Luteolin is capable of protecting the myocardium against IR injury. The actions of luteolin are at least partly mediated through downregulation of NO production and its own antioxidant properties.
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Liao et al. (2010) studied Myocardial ischemia-reperfusion injury. Luteolin vs. Vehicle (0.01% DMSO in normal saline) was evaluated on Myocardial infarct size (percentage of area at risk) (p=<0.05). Pretreatment with 10 μg/kg luteolin significantly reduced myocardial infarct size from 18.6% to 10.0% of the area at risk and eliminated mortality during ischemia-reperfusion injury in rats.
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