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首页> 外文期刊>Cellular Physiology and Biochemistry >AMPK Contributes to Cardioprotective Effects of Pterostilbene Against Myocardial Ischemia- Reperfusion Injury in Diabetic Rats by Suppressing Cardiac Oxidative Stress and Apoptosis
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AMPK Contributes to Cardioprotective Effects of Pterostilbene Against Myocardial Ischemia- Reperfusion Injury in Diabetic Rats by Suppressing Cardiac Oxidative Stress and Apoptosis

机译：AMPK通过抑制心脏的氧化应激和细胞凋亡，从而增强了蝶呤对糖尿病大鼠心肌缺血-再灌注损伤的保护作用。

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Background/Aims Pterostilbene (PT) exerts antidiabetic effects by decreasing blood glucose and modulating lipid metabolism and has been shown to attenuate myocardial ischemia-reperfusion (IR) injury in non-diabetic subjects. However, whether PT can protect against myocardial IR injury in diabetes is unknown. AMPK stimulation is indispensable in offering cardioprotection against myocardial IR injury in diabetes by limiting cardiac apoptosis. Thus, we hypothesized that PT may confer protection against myocardial IR injury in diabetes via AMPK activation. Methods Sprague-Dawley rats at eight weeks of diabetes induction (induced by an intravenous dose of 65 mg/kg streptozotocin) were administered with vehicle or PT (20 and 40 mg/kg/day, p.o.) for four weeks (starting from week 9 to 12). At the end of week 12, myocardial IR injury was induced by subjecting the diabetic rats to 30 minutes of coronary artery ligation and followed by 2 hours of reperfusion. In in vitro studies, rat primary cardiomyocytes were incubated with low glucose (LG, 5.5 mM) or high glucose (HG, 30 mM) and exposed to 45 minutes hypoxia and 2 hours reoxygenation in the presence or absence of PT (0.5 µM) or the AMPK inhibitor compound C (CC, 5 µM). Results PT significantly reduced post-ischemic cardiac infarct size, oxidative stress, plasma lactate dehydrogenase (LDH), creatine kinase-MB levels and apoptosis in diabetic rats. In cardiomyocytes, PT decreased hypoxia/ reoxygenation-induced oxidative stress, attenuated LDH and cleaved caspase3/caspase3 ratio and increased Bcl-2/Bax ratio and AMPK phosphorylation. However, CC administration blunted the cardioprotective effects of PT both in vivo and in vitro. Conclusion Suppressing cardiac oxidative stress and apoptosis via AMPK stimulation may represent a primary mechanism whereby pterostilbene attenuates diabetic myocardial IR injury.
机译：背景/目的蕨类植物（PT）通过降低血糖和调节脂质代谢发挥抗糖尿病作用，并已显示出可减轻非糖尿病受试者的心肌缺血-再灌注（IR）损伤。但是，PT是否可以预防糖尿病患者的心肌IR损伤尚不清楚。 AMPK刺激通过限制心脏凋亡来提供针对糖尿病的心肌IR损伤的心脏保护必不可少。因此，我们假设PT可以通过AMPK激活赋予糖尿病患者心肌IR损伤的保护作用。方法：在诱导糖尿病的八周（静脉内剂量65 mg / kg链脲佐菌素诱导）的Sprague-Dawley大鼠中，以媒介物或PT（20和40 mg / kg /天，口服）给药4周（从第9周开始）至12）。在第12周结束时，对糖尿病大鼠进行30分钟的冠状动脉结扎，然后再进行2小时的再灌注，从而诱发心肌IR损伤。在体外研究中，将大鼠原代心肌细胞与低葡萄糖（LG，5.5 mM）或高葡萄糖（HG，30 mM）孵育，并在存在或不存在PT（0.5 µM）或不存在PT的情况下暴露于缺氧45分钟和复氧2小时。 AMPK抑制剂化合物C（CC，5 µM）。结果PT显着降低了糖尿病大鼠的缺血性心肌梗死面积，氧化应激，血浆乳酸脱氢酶（LDH），肌酸激酶-MB水平和细胞凋亡。在心肌细胞中，PT降低了缺氧/复氧诱导的氧化应激，LDH减弱，caspase3 / caspase3比例降低，Bcl-2 / Bax比例和AMPK磷酸化增加。然而，CC施用在体内和体外均削弱了PT的心脏保护作用。结论通过AMPK刺激抑制心脏氧化应激和细胞凋亡可能是蝶形蝶烯减轻糖尿病心肌IR损伤的主要机制。

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