摘要
目的：探讨血清中IL-8对心肌缺血再灌注（MlR）组织中p53、Bcl-2基因的影响。方法建立大鼠心肌缺血再灌注模型，分为对照组和实验组，缺血30min后，再灌注2、4、8、12、24、48h．各时间点分别处死动物，取血备用。采用双抗体夹心酶联免疫吸附（ELISAj法，原位杂交法，原位末端标记染色等，检测IL-8，p53mRNA，bcl-2mRNA，和细胞凋亡。结果：血清中IL-8在IR2h即开始升高，12h达高峰。组织中p53在4h开始升高，24h达高峰。BU-2在8h开始升高-直持续到48h达高峰。血清JL-8早于组织p53表达，Bcl-2晚于p53表达，心肌细胞凋亡和p53mRNA表达时间相-致。结论：血清中IL-8增高介导了组织中p53的高表达，抑制了Bcr-2的作用，在MIR损伤中扮演了-个重要角色。
Abstract
Objective ： To study the singniticance of interleukin-8（IL-8）,p53mRNA and Bcl-2mRNA in myocardial infarction reperfusion（MIR） injury. Methods：Build up the big rat MIR the model, ising divided into the matched control and experimenting the group, after infarction 30 mins, then reperfusion to note 2,4,8,12,24,48 h, each time orders to sentence to death the animal respectively, taking the blood back up. the contents of IL-8,p53mRNA and Bcl-2mRNA were examined by ELISA, in situ hybridization and TEUNL techniques. Results：See from MIR time window, the IL-8 starts go up namely in the 2h of IR, the 12h reaches the high peak.The p53 starts go up in the 4h, the 24h reaches the high peak.The Bcl-2 starts go up in the 8h to had been keep on till the 48h.Early the IL-8 expresses in the p53, the nights Bcl-2s express in the p53, the myocardial apoptosis with the p53mRNA the expression time mutually.Conclusion： In the serum the IL-8 increase high lay to lead the organization in the p53 of high expression, repressed the function of the Bcl-2, played an important role in MIR hurt.
基金项目
本课题受河南省科技厅科技攻关重点资助(0524410058)
NETL
NSTL
维普
万方数据