心房颤动患者基质金属蛋白酶及细胞因子表达的研究  

Expression of Matrix Metalloproteinase and Cytokines During Atrial Fibrillation Investigation

作　　者：谭蓓[1] 张海澄[1] 高瑾[1] 李春[1] 刘元生[1] 郭继鸿[1] 

机构地区：[1]北京大学人民医院心内科,北京市100044

出　　处：《中国循环杂志》2007年第6期436-439,共4页Chinese Circulation Journal

基　　金：国家自然基金资助课题(项目编号30471710)

摘　　要：目的:通过酶联免疫吸附方法对心房颤动(房颤)患者血清基质金属蛋白酶(MMPs)及其内源性抑制剂金属蛋白酶组织抑制因子(TIMPs),以及细胞因子的表达进行定量研究。方法:选取85例患者,其中永久性房颤组25例,阵发性房颤组28例,窦性心律组32例。应用酶联免疫吸附方法检测患者血清中 MMP-1、MMP-2、MMP-7、MMP-9、TIMP-1、TIMP-2及转化生长因子β、肿瘤坏死因子、血小板源性因子、血管内皮生长因子、碱性成纤维细胞生长因子和胰岛素样生长因子含量。结果:MMP-1在阵发性房颤组较窦性心律组升高19.80%(P<0.05)。MMP-2在永久性房颤组较阵发性房颤组及窦性心律组分别升高59.18%和41.87%(P<0.05)。MMP-7、MMP-9及 TIMP-1在3组间无统计学差异(P>0.05)。TIMP-2在永久性房颤组及阵发性房颤组分别较窦性心律组下降22.0%和13.01%(P<0.05)。转化生长因子β在永久性房颤组较阵发性房颤组及实性心律组分别升高30.04%和20.83%(P<0.05)。肿瘤坏死因子α在永久性房颤组及阵发性房颤组较窦性心律组分别升高28.3%和15.65%(P<0.05)。碱性成纤维细胞生长因子在永久性房颤组及阵发性房颤组较窦性心律组分别升高4.45%和3.76%(P<0.05)。胰岛素样生长因子1在永久性房颤组较窦性心律组下降21.97%(P<0.05)。血小板源性因子及血管内皮生长因子在三组间无统计学差异(P>0.05)。结论:房颤时细胞因子调节 MMPs/TIMPs 系统导致胶原降解与合成失衡使细胞外基质重构,这可能是房颤时心房结构重构的机制之一,与房颤的发生和维持有关。Objective： To quantify the association of serum levels of matrix metalloproteinases （MMPs）, tissue inhibitors of metalloproteinases （T IMPs） ,and associated cytokines with atrial fibrillation（AF）. Methods ： Eighty five patients in our hospital were enrolled. Out of them 25 patients had permanent AF, 28 patients had paroxysmal AF, and 32 patients sinus rhythm. The serum levels of all markers were measured by ELISA. Results： MMP-1 significantly increased in paroxysmal AF group by 19. 80% （P 〈 0. 05 ）over sinus rhythm group. MMP-2 significantly increased in permanent AF group over paroxysmal AF group and sinus rhythm group by 59.18% and 41.87% （P 〈 0.05 ）, respectively. MMP-7, MMP-9 and TIMP-1 had no significant difference between 3 groups （ P 〉 0.05 ）. TIMP-2 significantly decreased in permanent AF group and paroxysmal AF group over sinus rhythm group by 22. 0% and 13.01% （ P 〈0. 05）, respectively. Transforming growth factor-β significantly increased in permanent AF group over paroxysmal AF and sinus rhythm groups by 30.04% and 20. 83% （ P 〈 0. 05 ）, respectively. Tumor necrosis factor -α significantly increased in permanent AF and paroxysmal AF groups over sinus rhythm group, by 28. 30% and 15.65% （P 〈0.05）, respectively. Basic fibroblast growth factor significantly increased in permanent AF and paroxysmal AF groups over sinus rhythm group by 4.45% and 3.76% （ P 〈 0. 05）, respectively. Insulin-like growth factor-1 significantly decreased in permanent AF group over sinus rhythm group by 21.97%. Platelet-derived growth factor and vascular endothelial growth factor had no significant difference between 3 groups （P 〉0.05）. Conclusion ： Inflammatory and remodeling cytokines can regulate MMP/TIMP system and disturb the balance of collagen synthesis and degradation, thus resulting in extracellular matrix remodeling. This may be one of the mechanisms of the atrial structural remodeling in atrial fibrillation, and it may be correlated with the initiat

关 键 词：心房颤动 结构重构 细胞因子 基质金属蛋白酶 金属蛋白酶组织抑制因子 

分 类 号：R541[医药卫生—心血管疾病]