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【目的】测定不同周期STZ诱导糖尿病生存信号改变对心肌缺血/再灌注(I/R)损伤及心肌细胞凋亡的影响。【方法】阻断和开放左冠状动脉前降支建立大鼠急性心肌I/R模型,用TTC染色,测定大鼠心肌I/R后梗死面积,用免疫印迹法定量分析代表心肌凋亡水平的caspase-3及代表细胞生存信号的磷酸化蛋白激酶B(P-Akt)的表达,用槽式电泳法测定硝基酪氨酸。【结果】在STZ处理后2周,糖尿病组(2WD)心肌梗死面积比相应周期对照组(2WC)明显缩小,STZ处理后16周(16WD),梗死面积比相应对照组(16WC)增加;P-Akt,在心肌的表达在2WD比2WC组增加35%,在16WD比16WC明显减少;超氧亚硝酸根离子(ONOO-)生成的标志性产物硝基酪氨酸(NT)在2WD组中较2WC组低约49%,但在16WD组中较16WC组显著增加;在缺血再灌注后,Caspase-3,在2WD组较2WC组中减少,而16WD组caspase-3较16WC组增加。【结论】STZ诱导糖尿病早期、晚期对心肌I/R损伤和细胞凋亡呈现相反的作用,这可能是由于早、晚期糖尿病相反的细胞生存信号改变而引起的。
【Objective】 To determine the effect of different periods of STZ-induced diabetes mellitus signal changes on myocardial ischemia / reperfusion (I / R) injury and cardiomyocyte apoptosis. 【Methods】 Acute myocardial I / R model was established by blocking and opening left anterior descending coronary artery. TTC staining was used to determine infarct area after myocardial I / R in rats. Quantitative analysis of the myocardial apoptosis by immunoblotting caspase-3 and phosphorylated protein kinase B (P-Akt), which represent cell survival signals, were determined by trough electrophoresis. 【Results】 The myocardial infarct size in diabetic group (2WD) was significantly reduced 2 weeks after STZ treatment compared with control group (2WC), and the area of infarction increased 16 weeks after STZ treatment (16WC); P -Akt, and the expression of Akt in myocardium increased 35% in 2WD group and 16WC in 16WD group compared with that in 2WD group. Nitrotyrosine (NT), a marker product produced by superoxide nitrite ion (ONOO-) Compared with 2WC group, it was about 49% lower than that in 2WC group, but significantly increased in 16WD group compared with 16WC group. Caspase-3 decreased in 2WD group and 2WC group, but increased in 16WD group compared with 16WC group after ischemia-reperfusion. 【Conclusion】 The early and late stages of STZ-induced diabetes have the opposite effects on myocardial I / R injury and apoptosis, which may be caused by the change of cell survival signal contrary to early and late stage diabetes.