摘要
目的应用免疫磁珠分离急性心肌梗死(AMI)及不稳定性心绞痛(UA)患者外周血中循环内皮细胞(CECs),探讨与炎性相关因子C反应蛋白质(CRP)、白细胞介素-6(IL-6)及肿瘤坏死因子α(TNFα)的相关性.方法 AMI及UA患者入院时取静脉血,用携带抗CD146抗体的免疫磁珠分离外周血CECs;遗传性血友病因子(vWF)、CD31免疫组化及透射电镜对分选细胞进行鉴定;应用Annexin V-FITC/PI检测其凋亡状态;酶联免疫法检测各种炎性相关因子.结果 AMI组(n=37)及UA组(n=12)的CECs数量[中位数(四分位数间距)分别为52(28～81.5)个/ml,29(18～61)个/ml]和血清CRP水平显著高于正常对照组(n=42,P<0.001).AMI加UA组剔除合并糖尿病的患者后(n=26),CECs数量与CRP水平仍显著高于对照组(P<0.001);AMI及UA组CECs的坏死率显著高于对照组(P<0.01);分选出的细胞vWF因子、CD31表达阳性;以研究对象作为整体分析时,CECs数量与CRP及IL-6水平呈显著相关(r=0.677, 0.316,P=0.000, 0.002),多元线性回归分析显示CRP水平及糖尿病对CECs数量有显著影响(OR=0.620, 0.164, 95%CI:3.985～6.751, 0.301～21.877, P=0.000, 0.044).结论 AMI及UA患者CECs数量增加与炎症引起的血管内皮损伤有关.
Objective To study the number of CECs in patients with acute myocardial infarction （AMI） and unstable angina （UA）, and to investigate its relationship with inflammatory related cytokines. Methods 37 patients with AMI, 12 patients with UA, and 42 health controls were studied. CECs were isolated from peripheral blood by using of immunomagnetic beads coated with antibodies against CD146. Their endothelial origin was confirmed by the positive labelling of yon Willebrand Factor （vWF）, CD31 and electron microscope. Annexin V-FITC/PI kit was used to measure the apoptosis of CECs. Inflammatory related cytokines were analyzed turbidimetrically or ELISA using of commercially available testing kit. Results CECs number was significantly higher in AMI and UA patients [ medians （ interquartile range） were 52（28 ～ 81.5）cells/ml and 29（ 18 ～ 61）cells/ml respectively] compared with health control [ 10. 5 （6 - 16. 5） cells/ml, P 〈 0. 001 ]. After excluding diabetes patients, the number of CECs and CRP in AMI and UA group （n = 26） were still significantly higher than controls. The necrotic rate of CECs in AMI and UA was significantly higher than controls （P 〈 0. 01 ）. Correlation analysis revealed a significant positive correlation between CECs and CRP, or IL-6 （ r = 0. 677, 0. 316, P = 0. 000, 0. 002 ）. The multivariate linear regression analysis showed that CRP and Diabetes increased the number of CECs significantly （ OR = 0. 620, 0. 164, 95% CI 3. 985 - 6. 751, 0. 301 - 21. 877, P = 0. 000, 0. 044 ） . Conclusion The mechanism responsible for the increase of CECs in acute coronary disease may be due to the vessel injury caused by inflammation.
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
2005年第7期631-635,共5页
Chinese Journal of Cardiology
基金
中国科学院知识创新工程(KJCX1-SW-07)
