{"title":"[Regulation of Mitochondria on Platelet Apoptosis and Activation].","authors":"Ying Hu, Li-Li Zha, Ke-Sheng Dai","doi":"10.19746/j.cnki.issn.1009-2137.2023.03.029","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To explore the regulation of mitochondria on platelet apoptosis and activation, and the relationship between platelet apoptosis and activation.</p><p><strong>Methods: </strong>Platelets were isolated from peripheral venous blood of healthy volunteers. Cyclosporin A (CsA), which has a protective effect on the function of platelet mitochondria, BAPTA, which can chelate calcium ions across membranes in platelets, and NAC, an antioxidant that reduces the level of intracellular reactive oxygen species, were selected for coincubation with washed platelets, respectively. By flow cytometry, platelet aggregator was used to detect the changes of platelet mitochondrial function and platelet activation indexes after different interventions.</p><p><strong>Results: </strong>H89, staurosporine, and A23187 led to platelet mitochondrial abnormalities, while CsA could effectively reverse the decline of platelet mitochondrial membrane potential caused by them. Antioxidant NAC could reverse platelet mitochondrial damage correspondingly, and completely reverse platelet shrinkage and phosphatidylserine eversion induced by H89. BAPTA, prostaglandin E1, acetylsalicylic acid and other inhibitors could not reverse the decline of platelet mitochondrial membrane potential.</p><p><strong>Conclusion: </strong>Mitochondrial function plays an important role in platelet apoptosis and activation. Abnormal mitochondrial function causes the imbalance of reduction/oxidation state in platelets, which leads to platelet apoptosis. Platelet apoptosis and activation are independent signal processes.</p>","PeriodicalId":35777,"journal":{"name":"中国实验血液学杂志","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"中国实验血液学杂志","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.19746/j.cnki.issn.1009-2137.2023.03.029","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: To explore the regulation of mitochondria on platelet apoptosis and activation, and the relationship between platelet apoptosis and activation.
Methods: Platelets were isolated from peripheral venous blood of healthy volunteers. Cyclosporin A (CsA), which has a protective effect on the function of platelet mitochondria, BAPTA, which can chelate calcium ions across membranes in platelets, and NAC, an antioxidant that reduces the level of intracellular reactive oxygen species, were selected for coincubation with washed platelets, respectively. By flow cytometry, platelet aggregator was used to detect the changes of platelet mitochondrial function and platelet activation indexes after different interventions.
Results: H89, staurosporine, and A23187 led to platelet mitochondrial abnormalities, while CsA could effectively reverse the decline of platelet mitochondrial membrane potential caused by them. Antioxidant NAC could reverse platelet mitochondrial damage correspondingly, and completely reverse platelet shrinkage and phosphatidylserine eversion induced by H89. BAPTA, prostaglandin E1, acetylsalicylic acid and other inhibitors could not reverse the decline of platelet mitochondrial membrane potential.
Conclusion: Mitochondrial function plays an important role in platelet apoptosis and activation. Abnormal mitochondrial function causes the imbalance of reduction/oxidation state in platelets, which leads to platelet apoptosis. Platelet apoptosis and activation are independent signal processes.
目的:探讨线粒体对血小板凋亡和活化的调控作用,以及血小板凋亡与活化的关系。方法:从健康志愿者外周静脉血中分离血小板。选择对血小板线粒体功能具有保护作用的环孢素A (Cyclosporin A, CsA)、对血小板内钙离子具有跨膜螯合作用的BAPTA和降低细胞内活性氧水平的抗氧化剂NAC分别与洗涤后的血小板共孵育。采用流式细胞术、血小板聚集仪检测不同干预措施后血小板线粒体功能及血小板活化指标的变化。结果:H89、staurosporine、A23187导致血小板线粒体异常,CsA可有效逆转其引起的血小板线粒体膜电位下降。抗氧化剂NAC可相应逆转血小板线粒体损伤,完全逆转H89诱导的血小板收缩和磷脂酰丝氨酸外翻。BAPTA、前列腺素E1、乙酰水杨酸等抑制剂均不能逆转血小板线粒体膜电位的下降。结论:线粒体功能在血小板凋亡和活化中起重要作用。线粒体功能异常导致血小板还原/氧化状态失衡,从而导致血小板凋亡。血小板凋亡和活化是两个独立的信号过程。