Cardioprotective Effects of Luteolin During Ischemia-Reperfusion Injury in Rats

被引:53
作者
Liao, Pei-Hu [1 ,2 ,3 ]
Hung, Li-Man [4 ]
Chen, Yi-Hung [5 ]
Kuan, Yu-Hsiang [1 ,2 ,3 ]
Zhang, Friedrich Bo-Yuan [6 ]
Lin, Ruey-Hseng [1 ,2 ,3 ]
Shih, Hung-Che [1 ,2 ,3 ]
Tsai, Shen-Kou [7 ]
Huang, Shiang-Suo [1 ,2 ,3 ]
机构
[1] Chung Shan Med Univ, Dept Pharmacol, Taichung 402, Taiwan
[2] Chung Shan Med Univ, Inst Med, Taichung 402, Taiwan
[3] Chung Shan Med Univ Hosp, Dept Pharm, Taichung 402, Taiwan
[4] Chang Gung Univ, Dept Life Sci, Coll Med, Tao Yuan, Taiwan
[5] China Med Univ, Grad Inst Acupuncture Sci, Taichung, Taiwan
[6] Mackay Mem Hosp, Dept Urol, Taipei, Taiwan
[7] Cheng Hsin Gen Hosp, Div Anesthesiol, Taipei, Taiwan
关键词
Cardioprotective agent; Ischemia; Luteolin; Nitric oxide; Reperfusion; MYOCARDIAL ISCHEMIA/REPERFUSION-INJURY; NITRIC-OXIDE; CORONARY-ARTERY; RESVERATROL; FLAVONOIDS; ARRHYTHMIAS; INFARCTION; REDUCTION; DAMAGE;
D O I
10.1253/circj.CJ-10-0381
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 15 min 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 (10 mu g/kg). Similarly, luteolin (1 mu g/kg) reduced ventricular arrhythmias and mortality during the reperfusion phase. Pretreatment with luteolin decreased plasma lactate dehydrogenase and nitric oxide (NO) levels. Luteolin (10 mu g/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. (Circ J 2011; 75: 443-450)
引用
收藏
页码:443 / 450
页数:8
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