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首页> 外文期刊>Aging cell. >Aging induces cardiac diastolic dysfunction, oxidative stress, accumulation of advanced glycation endproducts and protein modification.
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Aging induces cardiac diastolic dysfunction, oxidative stress, accumulation of advanced glycation endproducts and protein modification.

机译：衰老会引起心脏舒张功能障碍，氧化应激，晚期糖基化终产物的积累和蛋白质修饰。

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Summary Evidence suggests that aging, per se, is a major risk factor for cardiac dysfunction. Oxidative modification of cardiac proteins by non-enzymatic glycation, i.e. advanced glycation endproducts (AGEs), has been implicated as a causal factor in the aging process. This study was designed to examine the role of aging on cardiomyocyte contractile function, cardiac protein oxidation and oxidative modification. Mechanical properties were evaluated in ventricular myocytes from young (2-month) and aged (24-26-month) mice using a MyoCam(R) system. The mechanical indices evaluated were peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR90) and maximal velocity of shortening/relengthening (+/- dL/dt). Oxidative stress and protein damage were evaluated by glutathione and glutathione disulfide (GSH/GSSG) ratio and protein carbonyl content, respectively. Activation of NAD(P)H oxidase was determined by immunoblotting. Aged myocytes displayed a larger cell cross-sectional area, prolonged TR90,and normal PS, +/- dL/dt and TPS compared with young myocytes. Aged myocytes were less tolerant of high stimulus frequency (from 0.1 to 5 Hz) compared with young myocytes. Oxidative stress and protein oxidative damage were both elevated in the aging group associated with significantly enhanced p47(phox) but not gp91(phox) expression. In addition, level of cardiac AGEs was approximately 2.5-fold higher in aged hearts than young ones determined by AGEs-ELISA. A group of proteins with a molecular range between 50 and 75 kDa with pI of 4-7 was distinctively modified in aged heart using one- or two-dimension SDS gel electrophoresis analysis. These data demonstrate cardiac diastolic dysfunction and reduced stress tolerance in aged cardiac myocytes, which may be associated with enhanced cardiac oxidative damage, level of AGEs and protein modification by AGEs.
机译：总结证据表明，衰老本身是造成心脏功能障碍的主要危险因素。非酶糖基化，即高级糖基化终产物（AGEs）对心脏蛋白的氧化修饰，被认为是衰老过程中的一个成因。这项研究旨在检查衰老对心肌细胞收缩功能，心脏蛋白氧化和氧化修饰的作用。使用MyoCam系统评价了来自年轻（2个月）和年龄大（24-26个月）小鼠的心室肌细胞的机械性能。评估的机械指标为峰缩短（PS），到达PS的时间（TPS），达到90％的延长时间（TR90）和最大缩短/延长的速度（+/- dL / dt）。氧化应激和蛋白质损伤分别通过谷胱甘肽和谷胱甘肽二硫化物（GSH / GSSG）比和蛋白质羰基含量进行评估。通过免疫印迹确定NAD（P）H氧化酶的激活。与年轻的心肌细胞相比，老化的心肌细胞显示出更大的细胞横截面积，延长的TR90，正常的PS，+ /-dL / dt和TPS。与年轻的心肌细胞相比，老化的心肌细胞对高刺激频率（0.1至5 Hz）的耐受性较低。氧化应激和蛋白质氧化损伤均在衰老组中升高，与p47（phox）的表达显着增强有关，但与gp91（phox）的表达无关。此外，通过AGEs-ELISA测定，老年心脏中的心脏AGEs水平比年轻心脏高约2.5倍。使用一维或二维SDS凝胶电泳分析，一组年龄在50至75 kDa之间，pI为4-7的蛋白质被显着修饰。这些数据表明老年心脏心肌细胞的心脏舒张功能障碍和应激耐受性降低，这可能与增强的心脏氧化损伤，AGEs水平和AGEs蛋白修饰有关。

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