激光心肌血管重建术诱导热休克蛋白表达上调

HEAT SHOCK PROTEINS ARE INVOLVED IN CARDIOPROTECTION OF PERCUTANEOUS TRANSLUMINAL MYOCARDIAL LASER REVASCULARIZATION

为探讨经皮穿刺激光心肌血管重建术 (PTMR)的心脏保护作用及其保护机制 ,在猪原位心脏缺血再灌注 (I/R)模型上 ,采用TTC法观察PTMR对于I/R后心肌梗死范围的影响 ,以Westernblotting方法测定心肌组织内热休克蛋白 (HSP) 70和 86蛋白水平的变化 ,并进行相关分析。结果发现PTMR组动物心肌梗死面积明显缩小 ,其梗死面积为 (32± 3) % ,对照组为 (5 6± 7) % (P <0 .0 5 ) ;PTMR区域心肌组织内HSP70和HSP86蛋白的相对含量较对照组明显升高。PTMR术后 2 4h ,I/R所致心肌梗死面积与HSP70和HSP86蛋白水平呈显著负相关 (r =0 .5 6和 0 .5 1,P均 <0 .0 1)。上述实验结果提示 ,心肌组织诱导型HSPs表达的上调可能参与了PTMR的心脏保护作用。

To investigate the cardioprotective effect of percutaneous transluminal myocardial laser revascularization (PTMR) and its mechanism, in the ischemia/reperfusion (I/R) model of in vivo porcine heart, the effect of PTMR on myocardial infarct size (IS) was observed using TTC method,and expression of heat shock protein (HSP) 70 and 86 in myocardium was detected with Western blotting. It was found that PTMR significantly limited the myocardial IS induced by I/R (32%±3% vs 56%±7% in control group, P <0.01) and increased the relative protein content of HSP70 and HSP86 in myocardium treated with PTMR. The IS induced by I/R correlated negatively with the expression of HSP70 and HSP86 in myocardium treated with PTMR 24 hours afterwards ( r =0.56 and 0.51, respectively, P <0.01). The results suggested that the upregulation of inducible HSPs expression might be involved in the cardioprotective mechanism of PTMR.