摘要
目的探讨缺血和缺血再灌注后交界区心肌细胞Caspase-3mRNA的动态变化与药物影响的关系。方法建立家兔心肌缺血再灌注模型,分为缺血组、IR组、IR+ACDEVDCHO组、和假手术组4组,并设立缺血1.5h后再灌注2、4、8、12、24、48h6个时相点。采用荧光分析法检测Caspase3活性,原位末端标记法标记凋亡细胞,伊文蓝和TTC染色测定梗死范围。结果①缺血组与IR组相比,在各时间点后者的Caspase3上调,交界区凋亡细胞增多,梗死范围扩大,尤其在24h时,两者之间有显著性差异,P<0.01;②IR组与IR+ACDEVDCHO组相比,后者在各时间点均阻断了Caspase3酶活性,凋亡细胞减少,梗死范围缩小,尤其在24h两者之间有显著性差异,P<0.01;③在缺血组,IR组,IR+ACDEVDCHO组,3组中Caspase3酶活性、凋亡细胞数、心肌的梗死范围之间呈正相关。结论①缺血再灌注交界区激活Caspase3酶活性,使凋亡细胞增多,梗死范围扩大,比缺血组对心肌的影响更大。阻断Caspase3酶活性可下调凋亡细胞数目,使梗死范围缩小;②交界区Caspase3酶活性与凋亡细胞数量影响着心肌细胞梗死的发生发展与结构重建,为临床上治疗心肌梗死提供了一个时间窗和新策略。
Objective To study the relation that myocardial Caspase-3 mRNA with activity changes and medicine influence in regions after permanent ischemia and ischemia reperfusion. Methods Build up the domestic rabbit model of myocardial ischemia reperfusion. A total of 17 rabbits were divided into 4 groups, ischemia group, IR group, IR ＋ AC-DEVD-CHO group, and sham operation group. The ischemic model were observed at 1.5h after ischemia followed by reperfusion at 2,4,8,12,24 and 48h. Adopt the fluorescence analysis method to examine caspase-3 activities. The activity of Caspase-3,the apoptotic cardiomyocytes and the myocardial infarction area were determined by fluorescent assay,TUNEL method and TTC dyeing, respectively. Results ①Ischemia group and IR group compared, ordering in each time,the Caspase-3 of the latter is obviously up - adjusted, the boundary area of apoptotic cell enlarging,the infarction area extension, particularly at 24h, the difference significant, P 〈 0.01. ②IR group and IR ＋ AC-DEVD-CHO group compared, the obstruct of Caspase-3 activity at each time in latter, the apoptotic cell reduce, and the infarction area contract, particularly at 24h, P〈0.01. ③In isehemia group,IR group,and IR ＋ AC-DEVD-CHO group,there present positive relativity at the Caspase-3 activity,the count of apoptotie cells and the myocardial infarction area. Conclusion ①The boundary area of Isehemia reperfusion activate the activity of Caspase-3 ,make the apoptotie cell increase, the infarction area enlarge. The ischemia group influences larger to the myocardial. Stop the activity of Caspase-3 can make apoptotie cell number descend,the infarction area contract. ②The boundary area Caspase-3 activity and the apoptotie cell quantities affect the occurrence, development and structure reconstructions of the myocardial infarction,and provide a time window and new strategy for curing the myocardial infarction.
出处
《中原医刊》
2005年第18期3-5,共3页
Central Plains Medical Journal
