Caspase-3抑制剂对大鼠心肌缺血再灌注损伤后梗死范围的影响  

Effects of caspase-3 inhibitor on infarct size of rats with myocardial reperfusion injury

作　　者：徐强[1] 司良毅[1] 赵小兰[1] 张红[1] 唐维平[1] 

机构地区：[1]第三军医大学附属西南医院老年病科,重庆400038

出　　处：《第三军医大学学报》2003年第16期1450-1453,共4页Journal of Third Military Medical University

摘　　要：目的　探讨天冬氨酸特异的半胱氨酸蛋白酶 3 (Caspase 3 )抑制剂Ac DEVD CHO对大鼠心肌缺血再灌注(MIR)后心肌梗死范围的影响机制。方法　Wistar大鼠 13 2只 ,设立MIR组 ,DEVD组和假手术组并分设缺血 3 0min后再灌注 1、3、6、12及 2 4h 5个时相点。分别检测caspase 3活性、心肌细胞凋亡指数 (AI)、ICAM 1表达、PMNs浸润数和心肌梗死范围。结果　Caspase 3活性、心肌细胞AI随再灌注时间延长而增加 ,心肌细胞AI与caspase 3活性于再灌注 12h最高 ,其后基本维持在平台状态 ;ICAM 1表达、PMNs浸润数和心肌梗死范围随再灌注时间延长而增加 ,至 2 4h仍未见下降趋势。DEVD组上述指标虽也有相似增高趋势 ,但比MIR组明显减小 (P <0 .0 5 )。结论　Caspase 3抑制剂Ac DEVDObjective To study the effects of caspase 3 inhibitor Ac DEVD CHO on infarct size of rat with myocardial reperfusion injury. Methods A total of 132 Wistar rats were divided into 3 groups, myocardial ischemia reperfusion (MIR), DEVD and sham. The activity of caspase 3, myocardial apoptosis index(AI), expression of intercellular adhesion molecule 1(ICAM 1), count of polymorphonuclear neutrophils (PMNs) infiltration, and myocardial infarct size in each group were detected at 1, 3, 6, 12 and 24 h. Results Activity of caspase 3 and AI increased in a time dependent manner and reached the peak value at 12 h and then maintained at a stable level. Expression of ICAM 1, count of PMN infiltration, and myocardial infarct size also increased in a time dependent manner, but no decrement was found even at 24 h following reperfusion. Those indices mentioned above in DEVD group were significantly lower than those in MIR group ( P <0.05) though similar increasing tendency was found in both groups. Conclusion Caspase 3 inhibitor Ac DEVD CHO reduces myocardial infarct size by means of inhibiting myocardial apoptosis and infiltration of PMNs.

关 键 词：心肌缺血 再灌注损伤 CASPASE-3 抑制剂 细胞凋亡 细胞粘附分子 中性粒细胞 大鼠 心肌梗死范围 

分 类 号：R654.1[医药卫生—外科学] R322.11[医药卫生—临床医学]