柚皮素对心肌缺血再灌注损伤的保护作用

The Protective Effect of Naringenin on Myocardial Ischemia Reperfusion Injury

柚皮素（naringenin, Nari）具有抗氧化和抗动脉粥样硬化的效应,并能激活ATP敏感性钾离子通道（KATP）以给心脏提供保护。为了探究Nari对心脏保护的机制,本研究选取成年雄性SD大鼠为研究对象,并将大鼠分为4组：对照组、NARI组、NARI＋格列本脲（GLI）组和NARI＋5-羟基癸酸（5-HD）组。将实验小鼠的心脏分离,Langendorff灌流,缺血处理30 min,然后再灌注60 min,测定其左心室压力、冠脉流出液中乳酸脱氢酶（LDH）、心肌超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量以及测量心肌梗死面积。结果发现,2.5μmol/L以上浓度的Nari能够促进左心室功能恢复,冠脉流出液中LDH降低,心肌梗死面积明显减少,说明Nari可增加心肌SOD活性,并减少心肌MDA含量,同时Nari的这种心脏保护作用可被GLI和5-HD阻断。研究证明,Nari在缺血再灌注损伤时具有心脏保护作用,其机制可能与通过激活细胞和线粒体膜KATP通道发挥增强心肌抗氧化的能力有关。

Naringenin （Nari） has antioxidative and anti-atherosclerosis effects, and activation of ATP-sensitive potassium channel （KATP） can offer a cardiac protection. In order to explore the mechanism of Nari＇s cardio- protection, adult male Sprague-Dawley rats were selected as the study subjects, and the rats were divided into four groups： control group, NARI group, NARI＋glibenclamide （GLI） group, and NARI＋5-Hydroxydecanoic acid （5-HD） group. The hearts of the experimental mice were isolated, Langendorffperfused, ischemic for 30 minutes, and then reperfused for 60 minutes. The left ventricular pressure, lactate dehydrogenase （LDH）, myocardial superoxide dismutase （SOD） activity, malondialdehyde （MDA） content, and myocardial infarct size were measured. The results showed that Nari above 2.5 μmol/L could promote the recovery of left ventricular function, decrease LDH in coronary effluent, and significantly reduce myocardial infarct size. This result indicates that Nari can increase myocardial SOD activity and reduce myocardial MDA content, while Nari＇s cardioprotective effect can be blocked by GLI and 5-HD. In conclusion, Nari has a cardioprotective effect on ischemia-reperfusion injury, and its mechanism may be related to its ability to enhance myocardial antioxidant activity by activating cells and the mitochondrial membrane KATP channel.