论文部分内容阅读
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 investigate the level of chemokine CCL2 in plasma and platelets in patients with acute ST-elevation myocardial infarction (STEMI) and its effect on P65 and IκBα in platelet nuclear factor-κB (NF-κB) signaling pathway. Methods: Fifty STEMI patients and 50 normal control subjects from CCU of Shenyang Military Region General Hospital from October 2015 to January 2016 were recruited. The levels of CCL2 in plasma were detected by ELISA. The levels of CCL2 and CCR2 . Western blot was used to detect the expression of p65 and IκBα in platelets stimulated by CCL2, and then pretreatment of platelets with CCR2 antagonist RS201895 and Bay11-7082, an inhibitor of NF-κB signaling pathway. The platelets were stimulated with CCL2 to detect the expression of p65 and IκBα . Results: The plasma concentration of CCL2 in STEMI patients was 222 ± 98 pg / m L and the plasma CCL2 concentration in normal controls was 162 ± 24 pg / m L, which was significantly lower than that in STEMI patients (P <0.01). The expression of CCL2 and CCR2 in platelets of STEMI patients was significantly higher than that of the normal controls (P <0.01). After CCL2 stimulation, the level of p P65 in platelets increased and the level of IκBα decreased (P <0.01). Before platelet stimulation with CCL2, the levels of p P65 and IκBα were increased after platelet pretreatment with RS201895 or Bay11-7082 P <0.01). Conclusion: The expression of CCL2 in plasma and platelets of patients with STEMI is increased. CCL2 / CCR2 may affect platelet function through NF-κB signaling pathway and may be involved in thrombosis.