通心络对活化血小板诱导人脐静脉内皮细胞的保护作用

被引:11
作者
刘红利 [1 ]
位庚 [2 ,3 ]
李红蓉 [2 ]
陈檬 [2 ,4 ]
王宏涛 [3 ,4 ]
机构
[1] 南京中医药大学
[2] 河北以岭医药研究院
[3] 国家中医药管理局重点研究室(心脑血管络病)
[4] 河北省络病重点实验室
关键词
通心络; 血小板; 人脐静脉内皮细胞; CD40L;
D O I
暂无
中图分类号
R285 [中药药理学];
学科分类号
100806 [中药药理学];
摘要
目的研究通心络对活化血小板诱导人脐静脉内皮细胞损伤的保护作用及白细胞分化抗原40配体(CD40L)在此损伤过程中的作用。方法取健康人新鲜血,离心获取血小板悬液,二磷酸腺苷(ADP)诱导活化,应用活细胞成像系统动态观察血小板形态变化、酶联免疫吸附试验(ELISA)测可溶性CD40L(s CD40L)表达;将静息血小板和活化血小板的上清液分别与人脐静脉内皮细胞株(HUVEC)共培养12 h,同时设正常组、阴性对照组、CD40L单克隆抗体组、通心络组。采用四唑化合物电子耦联显色法(MTS法)检测HUVEC生存活性,ELISA法检测HUVEC炎性细胞因子细胞间黏附分子-1(s ICAM-1)、E-选择素(E-selectin)、荧光检测法测HUVEC线粒体膜电位。结果 ADP诱导激活的血小板高表达可溶性CD40L,血小板形态由圆形变为不规则,并有胞浆内物质释放。活化血小板上清液诱导HUVEC生存活性下降,炎症因子s ICAM-1、E-selectin分泌显著升高,且HUVEC线粒体膜电位下降。通心络及CD40L单抗预处理HUVEC,与活化组比较,均能显著降低s ICAM-1、E-selectin的表达,升高HUVEC线粒体膜电位,改善HUVEC生存活性。结论体外活化的血小板能够启动血小板-内皮细胞炎症反应,诱导HUVEC功能障碍,其机制可能是通过CD40L-CD40起作用。通心络抑制活化血小板对HUVEC的损伤,对血小板、内皮细胞具有保护作用。
引用
收藏
页码:2035 / 2038
页数:4
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