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首页> 外文期刊>Bulletin of experimental biology and medicine >Effect of NAD on recovery of adenine nucleotide pool, phosphorylation potential, and stimulation of apoptosis during late period of reperfusion damage to myocardium.
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Effect of NAD on recovery of adenine nucleotide pool, phosphorylation potential, and stimulation of apoptosis during late period of reperfusion damage to myocardium.

机译:NAD对心肌再灌注损伤后期腺嘌呤核苷酸库的恢复,磷酸化潜力和细胞凋亡刺激的影响。

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The system of energy supply in the myocardium of the left and right ventricles did not recover after short-term circulatory disturbances. ATP synthesis decreased in parallel with activation of poly-(ADP-ribose)-polymerase in the ischemic region of the right ventricle, extra-ischemic region, and in the left ventricle by 5.85, 5.4, and 2.2 times, respectively. Intravenous injection of NAD immediately after blood flow resumption in the subacute period of ischemia-reperfusion damage virtually completely normalized the pool of adenine nucleotides, energy change of the adenine nucleotide system, and phosphorylation potential. Exogenous NAD inhibited activity of poly-(ADP-ribose)-polymerase in the ischemic region of the right ventricle, extra-ischemic region, and in the ischemic region of the left ventricle by 2.4, 2.9, and 1.52 times, respectively. We hypothesize that NAD acts as a regulator of signal mechanism of apoptosis induction during ischemia-reperfusion damages to the myocardium.
机译:短期循环障碍后,左右心室心肌的能量供应系统未恢复。与右心室缺血区域,缺血外区域和左心室中的聚(ADP-核糖)-聚合酶激活同时,ATP合成分别降低了5.85、5.4和2.2倍。在亚急性缺血/再灌注损伤后的血流恢复后立即静脉注射NAD,实际上使腺嘌呤核苷酸池,腺嘌呤核苷酸系统的能量变化和磷酸化潜力完全正常化。外源NAD抑制聚(ADP-核糖)-聚合酶在右心室缺血区域,缺血外区域和左心室缺血区域的活性分别为2.4、2.9和1.52倍。我们假设,NAD在心肌缺血再灌注损伤过程中起凋亡诱导信号机制的调节作用。

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