急性心肌梗死患者CCL2/CCR2与血小板聚集率的关系
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摘要
目的:研究急性心肌梗死(AMI)患者CC类趋化因子配体2 (CCL2)及其受体(CCR2)表达与血小板聚集率的关系。方法:选择我院冠心病监护病房收治的60例AMI患者作为AMI组,另60例体检健康者作为正常对照组。检测两组血浆CCL2水平,及冠脉血栓组织中血小板CCL2和CCR2蛋白表达和定位情况,比较正常对照组CCL2刺激前后活化的糖蛋白Ⅱb/Ⅲa复合物(PAC-1)和CD62p水平变化,及不同CCL2水平对血小板聚集率的影响。结果:与正常对照组比较,AMI组血浆CCL2 [(159.63±54.32)pg/ml比(218.79±76.34)pg/ml]、血小板CCL2 [(0.86±0.38)比(2.05±0.59)]和CCR2 [(0.93±0.42)比(2.67±0.51)]蛋白表达均显著升高(P均=0.001),CCL2/CCR2与CD62p在AMI患者中存在共定位表达关系。与CCL2刺激前比较,正常对照组经CCL2刺激后PAC-1 [(9.83±3.14)%比(18.96±4.25)%]和CD62p[(5.08±1.16)%比(8.33±1.89)%]表达均显著升高(P均=0.001)。当CCL2浓度≥100ng/ml时起,血小板最大聚集率均显著高于CCL2浓度为0时水平(P均=0.001)。结论:急性心肌梗死患者CCL2/CCR2表达与血小板聚集率关系密切,CCL2/CCR2可能通过影响血小板聚集率,参与疾病进展。
Objective:To explore relationship among expressions of CC type chemokine ligand 2(CCL2)and its receptor(CCR2)and platelet aggregation rate in patients with acute myocardial infarction(AMI).Methods:A total of 60 AMI patients treated in our coronary care unit were regarded as AMI group,another 60 healthy subjects undergoing physical examination were enrolled as normal control group.Plasma CCL2 level,expressions and location of platelet CCL2 and CCR2 in coronary thrombus tissue were measured in two groups.Changes of activated glycoproteinⅡb/Ⅲa compound(PAC-1)and CD62 p levels,and influence of different CCL2 level on platelet aggregation rate(PAR)were compared in normal control group before and after CCL2 stimulus.Results:Compared with normal control group,there were significant rise in plasma CCL2 level[(159.63±54.32)pg/ml vs.(218.79±76.34)pg/ml],expressions of platelet CCL2 [(0.86±0.38)vs.(2.05±0.59)]and CCR2 protein [(0.93±0.42)vs.(2.67±0.51)]in AMI group(P=0.001 all),co-location expression relationship existed between CCL2/CCR2 and CD62 p in AMI patients.Compared with before CCL2 stimulus,there were significant rise in expressions of PAC-1[(9.83±3.14)% vs.(18.96±4.25)%]and CD62 p [(5.08±1.16)% vs.(8.33±1.89)%]in normal control group after CCL2 stimulus,P=0.001 both.When CCL2≥100 ng/ml,maximum PAR was significantly higher than that of CCL2=0 ng/ml level,P=0.001 all.Conclusion:Expression of CCL2/CCR2 is closely associated with platelet aggregation rate in AMI patients.CCL2/CCR2 may be involved in disease progress via affecting platelet aggregation rate.
Objective:To explore relationship among expressions of CC type chemokine ligand 2(CCL2)and its receptor(CCR2)and platelet aggregation rate in patients with acute myocardial infarction(AMI).Methods:A total of 60 AMI patients treated in our coronary care unit were regarded as AMI group,another 60 healthy subjects undergoing physical examination were enrolled as normal control group.Plasma CCL2 level,expressions and location of platelet CCL2 and CCR2 in coronary thrombus tissue were measured in two groups.Changes of activated glycoproteinⅡb/Ⅲa compound(PAC-1)and CD62 p levels,and influence of different CCL2 level on platelet aggregation rate(PAR)were compared in normal control group before and after CCL2 stimulus.Results:Compared with normal control group,there were significant rise in plasma CCL2 level[(159.63±54.32)pg/ml vs.(218.79±76.34)pg/ml],expressions of platelet CCL2 [(0.86±0.38)vs.(2.05±0.59)]and CCR2 protein [(0.93±0.42)vs.(2.67±0.51)]in AMI group(P=0.001 all),co-location expression relationship existed between CCL2/CCR2 and CD62 p in AMI patients.Compared with before CCL2 stimulus,there were significant rise in expressions of PAC-1[(9.83±3.14)% vs.(18.96±4.25)%]and CD62 p [(5.08±1.16)% vs.(8.33±1.89)%]in normal control group after CCL2 stimulus,P=0.001 both.When CCL2≥100 ng/ml,maximum PAR was significantly higher than that of CCL2=0 ng/ml level,P=0.001 all.Conclusion:Expression of CCL2/CCR2 is closely associated with platelet aggregation rate in AMI patients.CCL2/CCR2 may be involved in disease progress via affecting platelet aggregation rate.
引文
[1]郭琳娟,洪葵.氯吡格雷抵抗的影响因素[J].临床心血管病杂志,2015,9(11):1150-1154.
[2]杜成林,侯铮,黄骥.冠心病患者经皮冠状动脉介入术治疗后血浆IL-12、MCP-1的水平变化[J].医学临床研究,2017,34(1):67-69.
[3]刘丹,田孝祥,张效林,等.趋化因子CCL2对人脐静脉内皮细胞ICAM-1表达的影响[J].现代生物医学进展,2016,16(26):5024-5027.
[4]中华医学会心血管病学分会.急性心肌梗死诊断和治疗指南[J].中华心血管病杂志,2001,16(6):407-422.
[5]曹禹,张效林,田孝祥,等.STEMI患者趋化因子CCL2的变化及其对NF-κB信号通路中P65和ⅠκBα的影响[J].中国循环杂志,2016,31(z1):31-32.
[6]杨丽霞,郭瑞威,齐峰,等.单核细胞趋化蛋白-2518G/A基因多态性与冠心病的关系[J].中华老年多器官疾病杂志,2012,11(4):273-276.
[7]张子为,陆文彬,汤勇,等.趋化因子诱饵受体D6在心肌梗死后心肌重塑中的作用及机制研究[J].东南大学学报(医学版),2015,23(1):59-64.
[8]于洪志,吴琦,武俊平,等.低分子量肝素和尿激酶对急性肺栓塞模型兔单核细胞趋化蛋白-1的影响[J].中华结核和呼吸杂志,2014,37(6):437-441.
[9]Wasiluk A,Mantur M,Kemona H,et al.Platelet expression of CD62Pin hypotrophic newborns[J].Platelets,2012,23(2):161-165.
[10]齐茗,王晨霞.血小板活化标志物CD62P、PAC-1与心血管病关系研究的进展[J].心血管康复医学杂志,2014,23(1):98-100.
[11]李子健.G蛋白偶联受体信号新调控机制[J].中国病理生理杂志,2015,15(10):1907-1907.
[12]陈杰民,兰军,涂昌,等.RNA干扰GPR14对自发性高血压大鼠血压和心血管重构的影响[J].临床和实验医学杂志,2012,11(1):1-3.
[13]蔡百桢,叶峰,罗明英,等.兔后肢高血流切应力诱导的侧支血管CCR2的表达及其与单核/巨噬细胞的关系[J].中国动脉硬化杂志,2015,23(11):1089-1092.
[14]张月明,谭荣玲.血清中PAC-1和CD62p水平在诊断及预测急性脑梗死患者病情程度中的应用价值[J].河北医学,2014,9(11):1840-1842.
[15]王国瑜,周广喜.大动脉粥样硬化性卒中与脑小血管病患者血小板PAC-1、CD62P阳性率和血清血小板因子4水平的差异[J].国际脑血管病杂志,2011,19(2):95-100.
[2]杜成林,侯铮,黄骥.冠心病患者经皮冠状动脉介入术治疗后血浆IL-12、MCP-1的水平变化[J].医学临床研究,2017,34(1):67-69.
[3]刘丹,田孝祥,张效林,等.趋化因子CCL2对人脐静脉内皮细胞ICAM-1表达的影响[J].现代生物医学进展,2016,16(26):5024-5027.
[4]中华医学会心血管病学分会.急性心肌梗死诊断和治疗指南[J].中华心血管病杂志,2001,16(6):407-422.
[5]曹禹,张效林,田孝祥,等.STEMI患者趋化因子CCL2的变化及其对NF-κB信号通路中P65和ⅠκBα的影响[J].中国循环杂志,2016,31(z1):31-32.
[6]杨丽霞,郭瑞威,齐峰,等.单核细胞趋化蛋白-2518G/A基因多态性与冠心病的关系[J].中华老年多器官疾病杂志,2012,11(4):273-276.
[7]张子为,陆文彬,汤勇,等.趋化因子诱饵受体D6在心肌梗死后心肌重塑中的作用及机制研究[J].东南大学学报(医学版),2015,23(1):59-64.
[8]于洪志,吴琦,武俊平,等.低分子量肝素和尿激酶对急性肺栓塞模型兔单核细胞趋化蛋白-1的影响[J].中华结核和呼吸杂志,2014,37(6):437-441.
[9]Wasiluk A,Mantur M,Kemona H,et al.Platelet expression of CD62Pin hypotrophic newborns[J].Platelets,2012,23(2):161-165.
[10]齐茗,王晨霞.血小板活化标志物CD62P、PAC-1与心血管病关系研究的进展[J].心血管康复医学杂志,2014,23(1):98-100.
[11]李子健.G蛋白偶联受体信号新调控机制[J].中国病理生理杂志,2015,15(10):1907-1907.
[12]陈杰民,兰军,涂昌,等.RNA干扰GPR14对自发性高血压大鼠血压和心血管重构的影响[J].临床和实验医学杂志,2012,11(1):1-3.
[13]蔡百桢,叶峰,罗明英,等.兔后肢高血流切应力诱导的侧支血管CCR2的表达及其与单核/巨噬细胞的关系[J].中国动脉硬化杂志,2015,23(11):1089-1092.
[14]张月明,谭荣玲.血清中PAC-1和CD62p水平在诊断及预测急性脑梗死患者病情程度中的应用价值[J].河北医学,2014,9(11):1840-1842.
[15]王国瑜,周广喜.大动脉粥样硬化性卒中与脑小血管病患者血小板PAC-1、CD62P阳性率和血清血小板因子4水平的差异[J].国际脑血管病杂志,2011,19(2):95-100.