STEMI患者血浆和血小板CCL2水平及其对血小板NF-κB信号通路的影响

Levels of Chemokine CCL2 in the Plasma and Platelets of Patients with ST Elevation Myocardial Infarction and Its Effect on the Signal Pathway of Nuclear Factor Kappa B in the Platelets

目的:研究急性ST抬高型心肌梗死(STEMI)患者血浆和血小板中趋化因子CCL2的水平及其对血小板核因子κB(NF-κB)信号通路中P65和IκBα的影响。方法:选择2015年10月至2016年1月沈阳军区总医院CCU收治的STEMI患者50例及同期正常对照人群50例,采用ELISA检测其血浆中CCL2水平,western blot检测其血小板中CCL2和CCR2的表达;western blot检测经CCL2刺激后血小板中p P65和IκBα表达,进而应用CCR2拮抗剂RS201895及NF-κB信号通路抑制剂Bay11-7082预处理血小板,再应用CCL2刺激血小板,检测p P65和IκBα表达。结果:STEMI患者血浆CCL2浓度为222±98 pg/m L,正常对照组血浆CCL2浓度为162±24 pg/m L,较STEMI组显著降低,差异存在统计学意义(P<0.01)。STEMI患者血小板中CCL2和CCR2的表达较正常对照组明显增加(P<0.01)。经CCL2刺激后,血小板中p P65水平升高,IκBα水平降低(P<0.01);在CCL2刺激血小板之前,应用RS201895或Bay11-7082预处理血小板后,其p P65水平降低,IκBα水平升高(P<0.01)。结论:STEMI患者血浆及血小板中CCL2表达增高,CCL2/CCR2可能通过NF-κB信号通路影响血小板功能,参与血栓形成。

Objective： To study the expressions of chemokine CCL2 in the plasma and the platelets of patients with STEMI, and investigate the effect of CCL2 on P65 and IκBα of the platelets. Methods： 50 patients with STEMI who were admitted in the CCU of General Hospital of Shenyang Military Region from October 2015 to January 2016 and 50 healthy controls were enrolled. The plasma CCL2 concentration of patients with STEMI and healthy controls were detected by ELISA. The expressions of CCL2 and CCR2 in the platelets were detected by western blot; the phosphorylation of P65 and IκBα in the platelets were tested by western blot after CCL2 stimulation, or while CCR2 antagonist RS201895 and NF-κB signaling pathway inhibitor Bay11-7082 were pretreated on the platelets. Results：The plasma CCL2 concentration of STEMI patients and healthy controls were 222 ±98 pg/m L and 162±24 pg/m L, there were significant statistical differences between the two groups（P〈0.01）. Compared with control group, the expression of CCL2 and CCR2 in the platelets were significantly increased in STEMI patients（P〈0.01）. After the platelets were stimulated by CCL2, p P65 increased and IκBαdecreased（P〈0.01）; when RS201895 or Bay11-7082 treated before CCL2 stimulation, the phosphorylation of P65 decreased and IκBαincreased（P〈0.01）. Conclusions： The expression of CCL2 in plasma and platelets of patients with STEMI increased. CCL2/CCR2 might affect the functions of platelets through NF-κB signaling pathway and participate in the thrombosis.