摘要
目的检测急性冠状动脉综合征(ACS)患者外周血中血管紧张素Ⅱ1型受体自身抗体(AT1-AAs)、单核细胞趋化蛋白-1(MCP-1)及高敏C反应蛋白(hs-CRP)表达情况,探讨AT1-AAs表达与ACS发病及斑块稳定性的关系。方法选择临床确诊ACS患者(AGS组)、稳定型心绞痛(SAP)患者(SAP组)和健康体检者(对照组)各60例,人工合成血管紧张素Ⅱ1型受体细胞外第二环功能表位肽段,采用酶联免疫吸附试验(ELISA)法检测患者外周血中AT1-AAs阳性表达情况,并检测MCP-1、hs-CRP水平。结果ACS组、SAP组及对照组AT1-AAs阳性表达率分别为45.0%(27/60)、21.7%(13/60)和5.0%(3/60),ACS组、SAP组明显高于对照组,ACS组明显高于SAP组,差异有统计学意义(P〈0.01)。ACS组、SAP组MCP-1和hs-CRP明显高于对照组,ACS组明显高于SAP组,差异有统计学意义(P〈0.01)。ACS组及SAP组AT1-AAs阳性患者的MCP-1和hs-CRP均明显高于AT1-AAs阴性患者,差异有统计学意义(P〈0.01)。结论AT1-AAs可能参与ACS的发病过程,促进炎性因子表达可能是AT1-AAs导致ACS斑块不稳定的重要机制之一。
Objective To examine the expression of autoantibodies against angiotensin Ⅱ1 type 1 receptor (AT1-AAs), monocyte chemoattractant protein-1 ( MCP-1 ) and high-sensitivity C-reactive protein (hs-CRP) in patients of acute coronary syndrome (ACS), and study the role of AT1-AAs in plaque stability and pathogenesis of ACS. Methods Sixty patients with ACS were selected as ACS group,60 patients with stable angina pectoris (SAP) were selected as SAP group, and 60 healthy people were selected as control groups. The epitopes of the second extracellular loop of angiotensin Ⅱ1 type 1 receptor ( 165 - 191 ) were synthesized and used as antigen to screen the serum autoantibodies by enzyme-linked immunosorbent assay (ELISA). The peripheral blood levels of MCP-1 and hs-CRP were also evaluated. Results The positive rates of AT1-AAs in ACS group, SAP group and control group were 45.0% (27/60), 21.7% ( 13/60 ) and 5.0% (3/60) ,respectively. The positive rates of AT1-AAs in ACS group and SAP group were significantly higher than those in control group,the positive rate of AT1-AAs in ACS group was significantly higher than that in SAP group,and there were statistical differences (P 〈 0.01 ). The MCP-1 and hs-CRP levels in ACS group and SAP group were significantly higher than those in control group,the MCP-1 and hs-CRP levels in ACS group were significantly higher than those in SAP group, and there were statistical differences (P 〈 0.01 ).The MCP-1 and hs-CRP levels in AT1-AAs positive patients in ACS group and SAP group were significantly higher than those in AT1-AAs negative patients,and there were statistical differences (P 〈0.01). Conclusions AT1-AAs may play an important role in the pathogenesis of ACS. Inducing the expression of inflammatory factor through AT1-AAs maybe an important mechanism for plaque instability.
出处
《中国医师进修杂志》
2014年第19期10-12,共3页
Chinese Journal of Postgraduates of Medicine
基金
甘肃省科技计划(1308RJzA135)