CORM-2对LPS诱导的血小板造血系细胞特异性蛋白-1磷酸化调节的研究  

The Research of Regulation of LPS-induced HS1 Phosphorylation by CORM-2 in Platelet

作　　者：赵昌明[1] 许磊[1,2] 郭东风[1] 施琴[1] ZHAO Changming XU Lei GUO Dongfeng et al(Shanghai Pudong New Area Public Welfare Hospital 201318)

机构地区：[1]上海市浦东新区公利医院急诊科,201318 [2]上海国际医学中心ICU

出　　处：《医学理论与实践》2017年第7期955-957,共3页The Journal of Medical Theory and Practice

基　　金：浦东新区科技发展基金创新资金(PKJ2012-Y55)

摘　　要：目的:探讨脓毒症一氧化碳释放分子2(CORM-2)对脂多糖(LPS)诱导的造血系细胞特异性蛋白-1(HS1)磷酸化调节方法。方法:收集健康人血小板,使用LPS体外刺激血小板,同时加入CORM-2观察血小板黏附、聚集、释放功能的变化,并同时检测磷酸化HS1(p-HS1)蛋白水平的改变。结果:显示CORM-2对血小板的黏附、聚集和释放功能具有抑制作用,且差异具有统计意义(P<0.05),CORM-2对HS1磷酸化有较强的抑制作用。结论:CORM-2与血小板功能以及血小板HS1的活化密切相关,且有望成为脓毒症治疗的靶点。Objective：To explore the regulation of LPS-induced phosphorylationHS1 by CORM-2in sepsis.Methods：Platelets from healthy donors were collected and stimulated the platelet by LPS,meanwhile the CORM-2was added to detect the variation of platelet function and phosphorylation HS1.Results：The results showed CORM-2have ability to inhibit LPS-induced function of platelet in terms of edhesion,aggeration and release.And the Western Blot showed CORM-2can down regulat the HS1 phosphorylation significantly.Conclusion：CORM-2was closely related HS1 activation in LPS-induced platelet and it will be a target for sepsis therapy.

关 键 词：脓毒症 血小板 造血系细胞特异蛋白1 脂多糖 一氧化碳释放因子-2 磷酸化 

分 类 号：R446[医药卫生—诊断学]