巩固, 熊利泽, 侯立朝, 黄怡. 内毒素诱导lrg表达对大鼠急性缺血/再灌注心肌的保护作用机制[J]. 心脏杂志, 2010, 22(3): 357-360.
    引用本文: 巩固, 熊利泽, 侯立朝, 黄怡. 内毒素诱导lrg表达对大鼠急性缺血/再灌注心肌的保护作用机制[J]. 心脏杂志, 2010, 22(3): 357-360.
    Endotoxin protects rat heart of myocardial reperfusion by inducing expression of lrg[J]. Chinese Heart Journal, 2010, 22(3): 357-360.
    Citation: Endotoxin protects rat heart of myocardial reperfusion by inducing expression of lrg[J]. Chinese Heart Journal, 2010, 22(3): 357-360.

    内毒素诱导lrg表达对大鼠急性缺血/再灌注心肌的保护作用机制

    Endotoxin protects rat heart of myocardial reperfusion by inducing expression of lrg

    • 摘要: 目的: 通过测定大鼠急性心肌缺血/再灌注损伤模型中lrg表达水平与血浆降钙素基因相关肽(CGRP)、内皮素(ET-1)、肿瘤坏死因子-α(TNF-α)表达水平及心肌梗死面积的变化,探索内毒素对缺血/再灌注心肌保护的分子机制。方法: 将30只SD大鼠随机分为单纯缺血/再灌注模型组、内毒素预处理组和手术对照组,每组10只。采用戊巴比妥钠(40 mg/kg)腹腔注射麻醉大鼠,采用穿线结扎左冠状动脉前降支制备大鼠心肌缺血/再灌注模型。采用免疫印迹法结合图像分析软件半定量计算lrg分子表达水平的动态变化,放射免疫法测定血浆CGRP、ET-1和TNF-α浓度,用氯化三苯四唑(TTC)染色法和计算机图像分析系统计算心肌梗死面积。结果: 大鼠左冠状动脉前降支缺血/再灌注1.5 h内毒素预处理组血浆ET-1和血清TNF-α浓度较缺血/再灌注组显著降低,心肌梗死面积也显著缩小(P<0.01);而血浆CGRP浓度则显著增高(P<0.01)。结论: 内毒素预处理可诱导lrg分子表达水平上调,并显著降低ET-1而增加CGRP浓度,减小心肌梗死面积,对急性心肌梗死后再灌注心肌产生一定的保护效应。

       

      Abstract: AIM: To explore the protective mechanism of endotoxin in myocardial ischemia-reperfusion injury. METHODS: The total of 30 SD rats were subject to ischemia-reperfusion. Pentobarbital sodium (40 mg/kg) was intraperitoneally injected to anaesthetize rats, and threading ligation of left anterior descending coronary artery was performed to induce myocardial ischemia-reperfusion model. 10 rats were pretreated with endotoxin, another 10 received surgery, and the rest 10 were used as the controls. Western blot and image analysis software were employed to semi-quantitatively calculate the dynamic changes of lrg expression level. The changes of plasma CGRP, ET-1 and TNF-α concentration were measured by radioimmunoassay. With triphenyl tetrazolium chloride (TTC) staining and computer image analysis system, the area of myocardial infarction was calculated. RESULTS: In endotoxin-pretreated group, the levels of plasma ET-1 and serum TNF-α and the myocardial infarct size were significantly reduced at 1.5 h following ischemia-reperfusion, compared with those in the control group (P<0.01), whereas the expression of lrg and level of plasma CGRP were significantly increased (P<0.01). CONCLUSION: Endotoxin pretreatment can upregulate lrg expression to significantly reduce ET-1 level, increasing CGRP concentration and reducing myocardial infarct size of acute myocardial infarction, which suggests endotoxins protective effect in myocardial reperfusion.

       

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