急性冠状动脉综合征患者外周血β2 整合素 和Fractalkine 的表达水平及机制研究

Exploring the expression of β2 integrin and Fractalkine in acute coronary syndrome patients

摘要:

目的 观察急性冠状动脉综合征（ACS）患者外周血中β2 整合素和Fractalkine 的表达水平并 探讨其作用机制。方法 选取襄阳市中心医院收治的86 例ACS 患者，其中不稳定型心绞痛（UA）32 例，急 性心肌梗死（AMI）54 例，并以20 例冠状动脉造影正常的患者和28 例稳定型心绞痛（SAP）作为对照。采 用流式细胞技术检测外周血白细胞中的β2 整合素[LFA-1（CD11a/CD18）和Mac-1（CD11b/CD18）] 阳性细胞百分率，酶联免疫吸附法检测血清中Fractalkine、ICAM-1 的水平，Western blotting 检测外周血白 细胞中FAK、PKB 蛋白表达水平。结果 AMI 组和UA 组患者外周血白细胞中LFA-1、Mac-1 阳性细胞 百分率和FAK、PKB 蛋白水平高于正常组和SAP 组患者（P <0.05）。冠状动脉粥样硬化性心脏病患者血清 中Fractalkine、ICAM-1 水平较冠状动脉造影正常的患者升高（P <0.05）。AMI 组患者血清中Fractalkine、 ICAM-1 的水平高于正常组、UA 组及SAP 组患者（P <0.05）。结论 ACS 时外周循环中Fractalkine 释放增加， 与白细胞表面的受体结合促进β2 整合素及黏附分子活化，激活FAK-PI3K/PKB 信号通路参与ACS 的炎症反应。

Abstract:

Objective To observe the expression levels of β2 integrin and Fractalkine in peripheral blood of patients with acute coronary syndrome (ACS) and to explore the possible mechanism. Methods Totally 86 patients with ACS admitted to our hospital were enrolled, including 32 patients with unstable angina (UA) and 54 patients with acute myocardial infarction (AMI). Another 20 patients with normal coronary angiography and 28 patients with stable angina (SAP) were regarded as control. The percentage of β2 integrin LFA-1 (CD11a/CD18) and Mac-1 (CD11b/CD18) positive cells in peripheral blood leukocytes was detected by flow cytometry. The levels of Fractalkine and ICAM-1 in serum were detected by ELISA. The expression levels of FAK and Akt in peripheral blood leukocytes were assessed by Western blotting. Results The percentages of LFA-1, Mac-1 positive cells and the expression of FAK, PKB protein in peripheral blood leukocytes of AMI group and UA group were significantly higher than those of normal group and SAP group (P < 0.05). The levels of Fractalkine and ICAM-1 in patients with coronary heart disease were significantly higher than those with normal coronary angiography (P < 0.05). The levels of Fractalkine and ICAM-1 in the serum of patients with AMI were the highest in the four groups (P < 0.05). Conclusions Increased Fractalkine that released in the peripheral circulation during ACS binds to the receptors on the surface of leukocytes and promotes activation of β2 integrin and adhesion molecules. The FAK-PI3K/PKB signaling pathway was activated and participated in inflammatory responses of ACS.