• Pei-Hu Liao, Li-Man Hung, Yi-Hung Chen, Yu-Hsiang Kuan, Friedrich Bo-Yuan Zhang, Ruey-Hseng Lin, Hung-Che Shih, Shen-Kou Tsai, and Shiang-Suo Huang.
• Department of Pharmacology and Institute of Medicine, Chung Shan Medical University, Chung Shan Medical University Hospital, Taichung, Taiwan.
• Circ. J. 2011 Jan 1;75(2):443-50.

BackgroundAntioxidants 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 ResultsRats 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.ConclusionsLuteolin 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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