白细胞介素-1预适应对心肌缺血再灌注损伤的保护作用及机制

目的 :观察低剂量白细胞介素 1β(IL 1β)预适应能否诱导心肌延迟保护作用的产生 ,并探讨其发生机制。方法 :在大鼠心肌缺血预适应和培养心肌细胞缺氧预适应模型上 ,分别设缺血或缺氧预适应组、IL 1β 预适应 (ILPC)组和缺血再灌注 (I/R )组或缺氧复氧 (A/R)组 ,检测预适应后即刻 ,12h ,2 4h细胞间粘附分子 (ICAM 1)和热休克蛋白72(HSP72 )表达 ,以及中性粒细胞 (PMN )浸润数和超氧化物歧化酶 (SOD)含量 ,并观察预适应 12h和 2 4h后心肌梗死范围和心肌细胞存活率的变化规律。结果 :ILPC组与I/R组比较 ,预适应后 2 4h大鼠心肌ICAM 1的表达、PMN浸润数明显减少 ,心肌梗死范围缩小 (P <0 .0 5或P <0 .0 1) ;与A/R组比较 ,预适应后 2 4h培养心肌细胞存活率、SOD含量、HSP72 表达均显著增加 (P <0 .0 5 ) ,而预适应后即刻无显著差异 (P >0 .0 5 )。结论 :低剂量ILPC和缺血或缺氧预适应能够诱导心肌延迟保护的发生 ;其发生机制除了与HSP72 表达和SOD含量增加有关外 ,且与ICAM 1表达下降 ,减少PMN浸润也有密切关系

Protective effect of interleukin-1β preconditioning on myocardial ischemic/reperfusion injury and its mechanism

AIM: To observe the myocardial delayed protection of the low doses interleukin-1 β(IL-1 β) preconditioning (PC),and further explore its mechanism. METHODS:In the preconditioning model of ischemia in vivo and anoxia in culture myocardial cells, we set up groups as follows:ischemia/anoxia preconditioning group (IPC/APC), IL-1 β preconditioning group (ILPC), and only ischemia/reperfusion group(I/R) or anoxia/reoxygenation group (A/R),and determined the expressions of intercellar adhesion molecules(ICAM-1) and heat shock protein 72 (HSP 72),the number of polymorphonuclear leukocytes (PMNs) and the contents of superoxides dismutase (SOD), and observed the changes of the infarct size and the rate of cell livabilty after PC 0, 12, 24 h. RESULTS: In vivo, ICAM-1 expressions、PMNs infiltrations and infarct size were significantly decreased in ILPC groups than that in I/R group at 24 h after PC. In the cultured cell, the rate of cell livablities, the expressions of HSP 72 and SOD contents were remarkably increased as compared with A/R group at 24 h after PC, but no changes immediately after PC. CONCLUSION: Myocardial delayed protection can be induced by myocardial ischemic/anoxia and low doses of interleukin-1 β, and its mechanism is closely related to the decreased expressions of ICAM-1 and PMNs infiltration, besides of increased SOD contents and HSP 72 expressions.