急性心肌缺血损伤中PI3K/Akt信号通路表达的研究

来源 :卫生研究 | 被引量 : 0次 | 上传用户:initialD2004
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目的通过检测pAkt、Akt、Caspase3和p38在急性心肌缺血大鼠心肌与骨骼肌组织中的表达,探讨PI3K/Akt介导的信号通路对急性心肌缺血的影响。方法采用异丙肾上腺素(ISO)腹腔注射制备急性心肌缺血大鼠模型,检测心电图及血流动力学指标;采用免疫斑点试验与Western blot检测急性心肌缺血与正常大鼠的心肌与骨骼肌pAkt、Akt、Caspase3和p38的蛋白表达水平。结果与正常大鼠比较,模型组大鼠心电图S-T段下移≥0.1mv。pAkt(P<0.05)、Caspase3(P<0.05)和p38(P<0.05)蛋白表达水平升高。Akt表达水平与对照组比较变化不明显(P=0.477)。结论急性心肌缺血大鼠pAkt、Akt及相关凋亡分子Caspase3和p38的表达水平升高,Akt表达水平变化不明显。 Objective To investigate the effect of PI3K / Akt-mediated signal pathway on acute myocardial ischemia by detecting the expression of pAkt, Akt, Caspase3 and p38 in myocardium and skeletal muscle of rats with acute myocardial ischemia. Methods The rat model of acute myocardial ischemia was established by intraperitoneal injection of isoproterenol (ISO), and the electrocardiogram and hemodynamics indexes were detected. Immunodiffusion and Western blot were used to detect the expressions of myocardial and skeletal muscle in acute myocardial ischemia and normal rats pAkt, Akt, Caspase3 and p38 protein expression levels. Results Compared with normal rats, the S-T electrocardiogram of the model group was lowered ≥0.1 mv. pAkt (P <0.05), Caspase3 (P <0.05) and p38 (P <0.05). Akt expression levels compared with the control group did not change significantly (P = 0.477). Conclusions The expressions of pAkt, Akt and related apoptotic molecules Caspase3 and p38 in acute myocardial ischemia rats were increased, and the changes of Akt expression did not change obviously.
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