抗霉素A诱导血小板凋亡的分子机制研究
发布时间：2018-08-03 10:24
【摘要】：目的探讨抗霉素A(AMA)诱导血小板凋亡及其分子机制。方法取健康志愿者单采血小板,离心洗涤得到洗涤血小板,将洗涤血小板与不同浓度的AMA孵育后,流式细胞术检测线粒体跨膜电位(ΔΨm)去极化、磷脂酰丝氨酸(PS)暴露、细胞内活性氧(ROS)、线粒体ROS、P-选择素表达和整合素αⅡbβ3活化;Western blot法检测半胱氨酸天冬氨酸蛋白酶3(Caspase-3)的活化。在抑制试验中,先将洗涤血小板与线粒体靶向的ROS拮抗剂Mito-TEMPO预孵育,然后再与AMA孵育,流式细胞术检测相关凋亡指标。结果AMA剂量依赖性诱导血小板ΔΨm去极化、PS暴露、细胞内ROS和线粒体ROS升高以及Caspase-3活化;但是AMA不能诱导血小板活化。线粒体靶向的ROS拮抗剂抑制AMA诱导的血小板ΔΨm去极化、PS暴露、Caspase-3活化以及线粒体ROS的生成。结论 AMA能够诱导血小板发生凋亡,线粒体ROS可能在AMA诱导的血小板凋亡过程中起重要作用。
[Abstract]:Objective to investigate the apoptosis of platelets induced by anti-mycin A (AMA) and its molecular mechanism. Methods single platelet was collected from healthy volunteers and washed platelets were obtained by centrifugation. After incubating washed platelets with different concentrations of AMA, mitochondrial transmembrane potential (螖 蠄 m) depolarization and phosphatidyl serine (PS) exposure were detected by flow cytometry. The activation of cysteine aspartate protease 3 (Caspase-3) was detected by Western blot method with the activation of integrin 伪 鈪，
本文编号：2161447
[Abstract]:Objective to investigate the apoptosis of platelets induced by anti-mycin A (AMA) and its molecular mechanism. Methods single platelet was collected from healthy volunteers and washed platelets were obtained by centrifugation. After incubating washed platelets with different concentrations of AMA, mitochondrial transmembrane potential (螖 蠄 m) depolarization and phosphatidyl serine (PS) exposure were detected by flow cytometry. The activation of cysteine aspartate protease 3 (Caspase-3) was detected by Western blot method with the activation of integrin 伪 鈪，
本文编号：2161447
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