节点文献
猪骨骼肌缺血预适应降低心肌缺血再灌注后基质金属蛋白酶的表达
Remote preconditioning induced by skeletal muscle ischemia reduces matrix metalloproteinases expression in porcine myocardium
【摘要】 目的观察猪骨骼肌缺血预适应对心肌缺血再灌注后坏死面积及心肌MMP-2、MMP-9及TIMP-1的影响。方法10只小型猪被随机分为缺血再灌注(I/R)组和远端预适应(RP)组。采用非开胸法建立心脏I/R模型,通过球囊堵塞左股动脉造成骨骼肌短暂缺血。以三硝基四氮唑红确定心肌梗死范围;以免疫组化和RT-PCR法测I/R心肌中MMP-2、MMP-9和TIMP-1表达及骨骼肌RP对此的影响。结果与I/R组相比,骨骼肌RP明显减少心肌梗死范围。在缺血区,RP明显降低MMP-2和MMP-9的表达,增加TIMP-1表达(P<0.05)。且RP明显减弱MMP-2和MMP-9 mRNA的表达,增强TIMP-1的mRNA表达(P<0.05)。结论骨骼肌缺血预适应心肌不仅可减少心肌坏死范围,还可能对心肌间质产生保护作用。
【Abstract】 To determine the effect of skeletal muscle ischemic preconditioning on myocardial infarct area and matrix metalloproteinases(MMPs) in porcine myocardium following ischemia resperfusion(I/R). Ten pigs were divided into I/R group and remote preconditioning(RP) group.The myocardial infarct size was measured with triphenyl tetrazolium choride(TTC).MMP-2,MMP-9 and TIMP-1 of myocardium in different areas were observed by immunohistochemistry and RT-PCR. In I/R group,the myocardial infarct size,expressed as percentage of the ischemic myocardium was(51.1±2.3)% and it was reduced to(24.1±1.5)% in RP group(P< 0.05).Immunohistochemical studies showed that the expression of MMP-2 and MMP-9 was higher,and TIMP-1 was lower in I/R group in ischemic area than that in non-ischemic area(P<0.05).But expression of MMP-2 and MMP-9 decreased,and TIMP-1 increased in RP group than that in I/R group(P< 0.05).RT-PCR studies showed that expression of MMP-2 and MMP-9 mRNA became stronger,and expression of TIMP-1 mRNA became weaker in ischemic area than nonischemic area in I/R group(P< 0.05).But expression of MMP-2 and MMP-9 mRNA became weaker,and expression of TIMP-1 mRNA became stronger in RP group than that in I/R group(P< 0.05).RP induced by skeletal muscle ischemia not only reduce mycardial infarct size,but also be potential protection of cardiac matrix from degrading.
【Key words】 skeletal muscle; remote preconditioning; myocardial protection; matrix metalloproteinases;
- 【文献出处】 基础医学与临床 ,Basic & Clinical Medicine , 编辑部邮箱 ,2006年03期
- 【分类号】R363
- 【被引频次】2
- 【下载频次】103