生物光素减轻血小板抑制剂诱导的血小板功能障碍

    Biophotin alleviates platelet dysfunction induced by platelet inhibitors

    • 摘要:
      目的 研究生物光素对阿司匹林和氯吡格雷联合诱导血小板功能的影响。
      方法  以人血小板为研究对象,通过阿司匹林和氯吡格雷联合诱导人血小板损伤,将血小板分为对照组、模型组、生物光素组,采用流式细胞仪检测血小板中P-选择素(P-selectin,CD62P)的活化;电阻法检测血小板聚集;免疫荧光法检测血小板在纤维蛋白原上的黏附;酶联免疫吸附法检测血小板中CD62P、血小板活化因子(platelet-activating factor,PAF)的含量。
      结果  与对照组相比较,模型组抑制血小板表面CD62P的活化,抑制血小板聚集和黏附,减少血小板中CD62P、PAF的含量(均P<0.01);与模型组相比较,生物光素组增强血小板表面CD62P的活化(P<0.05),促进血小板聚集(P<0.05,P<0.01)和黏附(P<0.01),增加血小板中CD62P、PAF的含量(P<0.05)。
      结论  生物光素减轻阿司匹林和氯吡格雷联合诱导的人血小板功能障碍,有望减少长期服用抗血小板药的患者在创伤及围手术期的出血。

       

      Abstract:
      AIM To investigate the effect of biophotin on platelet function induced by the combined use of aspirin and clopidogrel.
      METHODS Human platelets were used for the research. Platelet injury was induced by combined use of aspirin and clopidogrel. Platelets were divided into control group, model group and biophotin group. Platelet activation marker CD62P was detected by flow cytometry, platelet aggregation was measured by impedance method, platelet adhesion on fibrinogen was assessed by immunofluorescence and the levels of CD62P and platelet activating factor (PAF) in platelets were measured by enzyme-linked immunosorbent assay.
      RESULTS Compared with the control group, the model group showed decreased surface activation of CD62P, inhibited platelet aggregation and adhesion and reduced levels of CD62P and PAF in platelets (all P<0.01). Compared with the model group, the biophotin group showed enhanced surface activation of CD62P (P<0.05), increased platelet aggregation (P<0.05, P<0.01) and adhesion (P<0.01) and higher levels of CD62P and PAF in platelets(P<0.05).
      CONCLUSION Biophotin alleviates platelet dysfunction induced by combined aspirin and clopidogrel, and it may help reduce the bleeding risk in patients on long-term antiplatelet therapy during trauma and perioperative periods.

       

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