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首页> 外文期刊>Free Radical Biology and Medicine: The Official Journal of the Oxygen Society >Evaluating the impact of diabetes and diabetic cardiomyopathy rat heart on the outcome of ischemia-reperfusion associated oxidative stress
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Evaluating the impact of diabetes and diabetic cardiomyopathy rat heart on the outcome of ischemia-reperfusion associated oxidative stress

机译:评估糖尿病和糖尿病心肌病大鼠心脏对缺血再灌注相关氧化应激的结果的影响

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Earlier literature underlines that oxidative stress plays a major role in the pathology of myocardial ischemia-reperfusion (I/R) injury, diabetic cardiomyopathy (DCM), diabetes mellitus (DM), fibrosis and hypertrophy which could adversely affect the normal cardiac function. However, the contributory role of oxidative stress in I/R pathology of heart with pre-existing abnormalities or diseases like DM and DCM remains to be explored. I/R injury was induced in normal (normal diet), DM (normal diet + streptozotocin: multiple low dose of 30 mg/kg) and DCM (high fat diet (40% fat) + streptozotocin: multiple low dose of 30 mg/kg) rat hearts using Langendorff isolated heart perfusion apparatus. Cardiac physiological recovery after I/R was assessed by hemodynamic parameters like LVDP, and LVSP, whereas cardiac injury was measured by tissue infarct size, and apoptosis, LDH, and CK release in coronary effluent. The oxidative stress was evaluated in myocardial homogenate, mitochondrial subpopulation, and microsomes. Reperfusing the ischemic DCM heart significantly deteriorated cardiac physiological recovery and elevated the cardiac injury (infarct size: 60%), compared to the control. But in DM heart, physiological recovery was prominent in the initial phase of reperfusion but deteriorated towards the end of reperfusion, supported by less infarct size. In addition, elevated lipid peroxidation (70% in DCM-I/R vs Sham) and impaired antioxidant enzymes (% decline vs Sham: GSH - 56% (DM), 63% (DCM); Catalase - 58% (DM), 35% (DCM); GPx - 19% (DM), 27% (DCM) and GR - 28% (DCM)) was observed in myocardial tissue from both DM and DCM. Interestingly, upon reperfusion, only normal heart showed significant deterioration in the antioxidant defense system. Collectively these results demonstrated that I/R induced oxidative stress is minimal in DM and DCM rat heart, despite high infarct size and low cardiac performance. This may be due to the prior adaptive modification in the antioxidant system associated with disease pathology.
机译:早期的文献强调,氧化应激在心肌缺血再灌注(I / R)损伤(DCM),糖尿病甲虫(DM),纤维化和肥大可能产生不利影响正常心脏功能的情况下发挥着重要作用。然而,氧化胁迫在I / R病理中的氧化胁迫对心脏预先存在的异常或DM和DCM等疾病的作用仍有待探讨。 I / R损伤在正常(正常饮食),DM(正常饮食+链脲佐菌素:多剂量为30mg / kg)和DCM(高脂饮食(40%脂肪)+链脲佐酮:多剂量为30mg / kg)鼠心使用Langendorff孤立的心脏灌注装置。通过LVDP等血流动力学参数评估I / R后的心脏生理恢复,而LVSP评估,而心脏损伤是通过组织梗塞大小测量的,并且冠状动脉出水中的凋亡,LDH和CK释放测量。在心肌匀浆,线粒体亚沉积物和微粒体中评价氧化应激。再灌注缺血性DCM心脏显着恶化,心脏生理恢复显着恶化,与控制相比,心脏损伤(梗塞大小:60%)升高。但在DM心脏中,在再灌注的初始阶段突出的生理恢复突出,但在再灌注结束时劣化,由少数梗塞尺寸较少。此外,脂质过氧化升高(DCM-I / R VS SHAM的70%)和抗氧化酶受损(%下降VS Sham:GSH - 56%(DM),63%(DCM);过氧化氢酶 - 58%(DM), 35%(DCM);在DM和DCM的心肌组织中观察到GPX - 19%(DM),27%(DCM)和GR-28%(DCM)。有趣的是,在再灌注后,只有正常的心脏在抗氧化防御系统中显示出显着恶化。尽管梗塞大小高,但梗塞大小高,因此总而言之,这些结果表明,I / R诱导的氧化应激在DM和DCM大鼠心脏中是最小的,尽管梗塞大小和低心性能。这可能是由于与疾病病理相关的抗氧化系统中的先前适应性修饰。

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