摘要
目的:探讨大鼠心肌梗死模型后不同时间受激活调节正常T细胞表达和分泌因子(RANTES)及其受体CCR5的时程变化.方法:结扎SD大鼠左冠状动脉前降支造成左室大面积心肌梗死,分别于术后1,2,4,8 wk测心功能,判断造模是否成功后开胸取心脏.运用实时荧光定量PCR和Western Blot蛋白印迹技术观察心肌梗死后不同时间点RANTES及其受体CCR5在mRNA和蛋白水平的表达变化.结果:心功能检测提示造模成功.和假手术组相比,心肌梗死组大鼠的RANTES,CCR5 mRNA水平变化:术后1 wk开始升高,4 wk时处于高峰(P<0.05),8 wk逐渐下调至正常水平;蛋白水平的变化与mR-NA的变化相似.结论:RANTES作为趋化因子,在心肌梗死早期对心肌的炎性反应进行调控.若能阻断RANTES对T细胞的趋化作用,可能减少心肌梗死后心肌炎性反应.
AIM： To investigate the changes of time course of regulated upon activation normal-cell expressed and secreted （RANTES） and its receptor chemokine （C-C motif） receptor 5 （CCR5） after myocardial infarction （MI） in rats. METHODS ： The MI model was induced by ligation of anterior descending coronary artery in SD rats. Heart function was tested 1,2, 4 and 8 weeks after surgery and the expressions of RANTES and CCR5 at mRNA and protein levels in the myocardium were detected respectively by real time RT-PCR and Western blot. RESULTS： Heart function test indicated that the MI model was successfully induced. The expressions of RANTES and CCR5 mRNA and protein increased I week after MI, reached the peak level in 4 weeks and were down-regulated 8 weeks post MI. Changes at protein level showed a similar pattern with those at mRNA level. CONCLUSION： As an inflammatory regulator and chemokine, RANTES can modulate inflammatory response after MI, thus contributing to the myocardial reparation after MI. Preventing the chemotaxis of RANTES and CCR5 on T cell in different stages after MI may reduce complications, ameliorate prognosis and increase the long-term survival rate.
出处
《第四军医大学学报》
北大核心
2009年第14期1278-1280,共3页
Journal of the Fourth Military Medical University
基金
广东省自然科学基金(8151001002000025)
