疏血通注射液抗血小板活化作用机制研究  

Study on the Mechanism of Antiplatelet Activation of Shuxuetong Injection

作　　者：马璐璐 张璐莎 李春晓 张丽媛 杨文杰 方乐玉 王倩怡 陈璐[2] 王虹 MA Lulu;ZHANG Lusha;LI Chunxiao;ZHANG Liyuan;YANG Wenjie;FANG Leyu;WANG Qianyi;CHEN Lu;WANG Hong(School of Integrative Medicine,Tianjin University of Traditional Chinese Medicine,Tianjin 301617,China;Key Lab of Pharmacology of TCM Formulae,Ministry of Education,Tianjin Key Lab of Chinese Medicine Pharmacology,Institute of Traditional Chinese Medicine,Tianjin University of Traditional Chinese Medicine,Tianjin 301617,China)

机构地区：[1]天津中医药大学中西医结合学院,天津301617 [2]方剂学教育部重点实验室,天津市中药药理学重点实验室,天津中医药大学中医药研究院,天津301617

出　　处：《中西医结合心脑血管病杂志》2021年第2期247-252,共6页Chinese Journal of Integrative Medicine on Cardio-Cerebrovascular Disease

基　　金：国家自然科学基金青年项目(No.81603329);国家国际科技合作专项基金资助项目(No.2015DFA30430)。

摘　　要：目的建立缺氧及氧化应激模型,探讨疏血通注射液抗血小板活化的作用机制。方法制备SD大鼠血小板悬液,建立1%O2诱导缺氧模型和500μmol/L过氧化氢诱导氧化应激模型。将血小板分为空白对照组、模型组、疏血通注射液低浓度组、疏血通注射液中浓度组、疏血通注射液高浓度组。采用比浊法检测血小板聚集;流式细胞术检测血小板CD62p的表达;蛋白免疫印迹法检测细胞外信号调节激酶5(ERK5)和p70核糖体蛋白S6激酶(P70S6K)的磷酸化蛋白表达;CM-H2DCFDA染色并检测血小板活性氧(ROS)的释放,观测血小板在纤维蛋白原上的黏附情况。结果与模型组相比,疏血通注射液可显著抑制血小板聚集,抑制血小板在纤维蛋白原上的黏附以及ROS的释放。同时疏血通注射液能有效抑制血小板CD62p的表达并抑制ERK5、P70S6K的磷酸化。结论疏血通注射液可能通过ERK5/P70S6K信号通路抑制血小板聚集、黏附、释放,从而抑制血栓形成。Objective To establish the model of hypoxia and oxidative stress,and to explore the mechanism of antiplatelet activation of Shuxuetong(SXT).Methods SD rats platelet suspension was prepared,hypoxia model was induced by 1%O2,and oxidation emergency model was induced by 500μmol/L H2O2.Platelets were divided into blank control group,model group,SXT low-concentration group,SXT medium-concentration group,and SXT high-concentration group.Platelet aggregation was detected by turbidimetry,platelet CD62p expression was detected by flow cytometry,and phosphorylated protein expression of ERK5 and P70S6K was detected by Western Blotting.CM-H2DCFDA staining was used to detect the release of platelet reactive oxygen species(ROS),and platelet adhesion to fibrinogen was observed.Results Compared with model group,SXT significantly inhibited platelet aggregation,platelet adhesion to fibrinogen,and ROS release.At the same time,SXT effectively inhibited the expression of platelet CD62p and the phosphorylation of ERK5 and P70S6K.Conclusion SXT may inhibit platelet aggregation,adhesion and release through ERK5/P70S6K signaling pathway,thus inhibiting thrombosis.

关 键 词：血小板活化 缺氧 氧化应激 疏血通注射液 实验研究 

分 类 号：R73[医药卫生—肿瘤]