论文部分内容阅读
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-2 in sepsis.Methods:Platelets from healthy donors were collected and stimulated the platelet by LPS,meanwhile the CORM-2 was added to detect the variation of platelet function and phosphorylation HS1.Results:The results showed CORM-2 have ability to inhibit LPS-induced function of platelet in terms of edhesion,aggeration and release.And the Western Blot showed CORM-2 can down regulat the HS1 phosphorylation significantly.Conclusion:CORM-2 was closely related HS1 activation in LPS-induced platelet and it will be a target for sepsis therapy.