首页|趋化因子RANTES及其受体CCR5在大鼠心肌梗死后的时程变化

趋化因子RANTES及其受体CCR5在大鼠心肌梗死后的时程变化

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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.
Changes of time course of RANTES and CCR5 following myocardial infarction in rats
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 ligetion 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 1 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 RANIES and CCR5 on T cell in different stages after MI may reduce complications, ameliorate prognosis and increase the long-term survival rate.

myocardial infarctionRANTKSreceptor,CCRSrats

王晓武、张卫达、袁彬彬、林曦、梅汝刚、王晓莉、李杰

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广州军区广州总医院心脏外科中心,广东,广州,510010

心肌梗塞 RANTES 受体,CCR5 大鼠

广东省自然科学基金

8151001002000025

2009

第四军医大学学报
第四军医大学

第四军医大学学报

CSTPCDCSCD北大核心
影响因子:0.599
ISSN:1000-2790
年,卷(期):2009.30(14)
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