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柚皮素通过激活大鼠ATP敏感性钾通道对缺血再灌注损伤的心脏保护作用。

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

作者信息

Meng Li-Min, Ma Hui-Jie, Guo Hui, Kong Qian-Qian, Zhang Yi

机构信息

a Department of Physiology, Hebei Medical University, Shijiazhuang 050017, PR China.

b Second Department of Cardiology, General Hospital of FengFeng Branch in Center Hebei Energy Sources Group, Handan 056200, PR China.

出版信息

Can J Physiol Pharmacol. 2016 Sep;94(9):973-8. doi: 10.1139/cjpp-2016-0008. Epub 2016 Apr 19.

Abstract

Naringenin (Nari) has antioxidative and anti-atherosclerosis effects, and activation of ATP-sensitive potassium channel (KATP) can offer cardiac protection. We hypothesized that Nari protects the heart against ischemia-reperfusion (I-R) injury through activation of KATP. 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 μmol/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.

摘要

柚皮素(Nari)具有抗氧化和抗动脉粥样硬化作用,而激活ATP敏感性钾通道(KATP)可提供心脏保护。我们推测Nari通过激活KATP来保护心脏免受缺血再灌注(I-R)损伤。成年雄性Sprague-Dawley大鼠的离体心脏先经历30分钟的全心缺血,然后再灌注60分钟(梗死面积测定时为120分钟)。心脏分别用Nari(NARI)、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)以及Nari加5-羟基癸酸(5-HD,一种线粒体膜ATP敏感性钾通道阻滞剂,NARI+5-HD)进行处理。测量左心室压力、冠状动脉流出液中的乳酸脱氢酶(LDH)、心肌中的超氧化物歧化酶(SOD)和丙二醛(MDA)以及心肌梗死面积。浓度高于2.5 μmol/L的Nari可改善左心室功能的恢复,降低冠状动脉流出液中的LDH,并减小心肌梗死面积。Nari处理的心肌中SOD活性增加而MDA减少。Nari的心脏保护作用被GLI和5-HD抵消。总之,Nari对I-R损伤具有心脏保护作用,这可能是通过激活细胞和线粒体膜中的ATP敏感性钾通道以及增强心肌抗氧化能力来实现的。

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