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The cardioprotective effect of naringenin against ischemia-reperfusion injury through activation of ATP-sensitive potassium channel in rat

机译:柚皮苷通过激活大鼠ATP敏感性钾通道对心肌缺血再灌注损伤的保护作用

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Naringenin (Nari) has antioxidative and anti-atherosclerosis effects, and activation of ATP-sensitive potassium channel (K-ATP) can offer cardiac protection. We hypothesized that Nari protects the heart against ischemia-reperfusion (I-R) injury through activation of K-ATP. Isolated hearts from adult male Sprague-Dawley rats experienced a 30-min global ischemia followed by 60-min reperfusion (120 min for the infarct size determination). The hearts were treated with Nari (NARI); Nari plus glibenclamide (GLI), a non-specific ATP-sensitive potassium channel blocker (NARI+GLI); and Nari plus 5-hydroxy decanoic acid (5-HD), a mitochondrial membrane ATP-sensitive potassium channel blocker (NARI+5-HD). The left ventricular pressure, lactate dehydrogenates (LDH) in coronary effluent, superoxide dismutase (SOD) and malondialdehyde (MDA) in myocardium, and myocardial infarct area were measured. Nari above 2.5 mu mol/L improved the recovery of left ventricular function, decreased LDH in coronary effluent, and reduced myocardial infarct area. The SOD activity was increased and MDA was decreased in Nari-treated myocardium. The cardioprotective effect of Nari was canceled by GLI and 5-HD. In conclusion, Nari has a cardioprotective effect against I-R injury, which may be carried out through activating ATP-sensitive potassium channels in both cell and mitochondrial membrane, and enhancing myocardial antioxidant capacity.
机译:柚皮素(Nari)具有抗氧化和抗动脉粥样硬化的作用,激活ATP敏感性钾通道(K-ATP)可以提供心脏保护作用。我们假设Nari通过激活K-ATP保护心脏免受缺血再灌注(I-R)损伤。成年雄性Sprague-Dawley大鼠的离体心脏经历了30分钟的整体缺血,然后再灌注60分钟(确定梗死面积120分钟)。心脏接受了Nari(NARI)治疗; Nari加格列本脲(GLI),一种非特异性ATP敏感性钾通道阻滞剂(NARI + GLI); Nari和5-羟基癸酸(5-HD),一种线粒体膜ATP敏感的钾通道阻滞剂(NARI + 5-HD)。测量左心室压力,冠状流出物中的乳酸脱氢盐(LDH),心肌中的超氧化物歧化酶(SOD)和丙二醛(MDA)以及心肌梗塞面积。 Nari高于2.5μmol / L可以改善左心室功能的恢复,减少冠状流出物中的LDH并减少心肌梗塞面积。在纳瑞治疗的心肌中,SOD活性增加而MDA降低。 GLI和5-HD取消了Nari的心脏保护作用。总之,Nari具有抗I-R损伤的心脏保护作用,可以通过激活细胞和线粒体膜中的ATP敏感钾通道并增强心肌的抗氧化能力来实现。

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