• 中国科学论文统计源期刊
  • 中国科技核心期刊
  • 美国化学文摘(CA)来源期刊
  • 日本科学技术振兴机构数据库(JST)

临床输血与检验 ›› 2025, Vol. 27 ›› Issue (1): 29-33.DOI: 10.3969/j.issn.1671-2587.2025.01.004

• 基础研究 • 上一篇    下一篇

吸烟对血小板数量和活化功能影响的实验研究*

刘贞, 汤龙海, 金一鸣, 徐子豪, 王明元   

  1. 苏州市中心血站,江苏苏州 215006
  • 收稿日期:2024-06-19 发布日期:2025-02-25
  • 通讯作者: 王明元,主要从事输血医学研究,(E-mail)mingyuan98@aliyun.com。
  • 作者简介:刘贞,主要从事输血免疫研究,(E-mail)dongludemeng@163.com。
  • 基金资助:
    *本课题受姑苏卫生人才科研项目(No.GSWS2023032)、苏州市科教兴卫(No. KJXW2022057)、苏州市重点学科(No.SZXK202118)、苏州市姑苏卫生人才计划(2023)035资助

Experimental Study on the Effects of Smoking on Platelet Count and Activation Function

LIU Zhen, TANG Longhai, JIN Yiming, XU Zihao, WANG Mingyuan   

  1. Suzhou Blood center, Suzhou 215006
  • Received:2024-06-19 Published:2025-02-25

摘要: 目的 探究吸烟人群血小板功能变化及原因,其可能诱发动脉粥样硬化的分子机制。方法 收集122例来自苏州市中心血站首次捐献单采血小板男性供者样本,根据献血者是否有吸烟史分为实验组(吸烟人群)和对照组(不吸烟人群)。比较两组人群血小板参数、血小板活化水平、后续血小板活化能力、血小板功能、ROS含量及线粒体功能。结果 与对照组相比,吸烟人群血小板MPV值和PDW值均显著升高(P<0.05),PLT数量无显著差异(P>0.05)。吸烟人群血小板表达更高水平的CD62P和αⅡbβ3(P<0.05),但凝血酶激活后,CD62P和αⅡbβ3的表达显著低于对照组(P<0.05),PF4后续释放不足(P<0.05)。此外,吸烟人群TEG检测结果表明其R值显著降低(P<0.05),MA值显著高于不吸烟人群(P<0.05),K值无显著差异(P>0.05)。尤为重要的是,吸烟人群血小板活性氧水平显著升高(P<0.05),线粒体功能探针表达显著降低(P<0.05)。结论 吸烟人群血小板基础活化增多,但凝血酶激活后血小板活化能力不足及释放功能受限,伴高水平ROS及线粒体功能受损。

关键词: 血小板, 血小板活化, ROS, 线粒体

Abstract: Objective To investigate the changes in platelet function among smokers and the underlying causes, as well as the potential molecular mechanisms that may induce atherosclerosis. Methods A total of 122 samples from first-time male platelet-apheresis donors at Suzhou Blood Center were collected, which were divided into an experimental group (smokers) and a control group (non-smokers) based on smoking history, with ensuing analyses on platelet parameters, platelet activation level, platelet function, reactive oxygen species (ROS) levels, and mitochondrial function. Results Compared with the control group, the mean platelet volume (MPV) and platelet distribution width (PDW) in smokers were significantly increased (P<0.05), while platelet count showed no significant difference (P>0.05). Smokers' platelets presented increased CD62P and αⅡbβ3 (P<0.05), but after thrombin activation, the expression of CD62P and αⅡbβ3 was significantly lower than that of the control group (P<0.05), and the subsequent release of PF4 was insufficient (P<0.05). Moreover, TEG test results in smokers indicated a significant decrease in the R value (P<0.05) and a significant increase in the MA value compared to non-smokers (P<0.05), with no significant difference in the K value (P>0.05). Importantly, the level of ROS in smokers' platelets was significantly elevated (P<0.05), and the expression of mitochondrial probes was significantly reduced (P<0.05). Conclusion Smokers exhibit basal platelet activation, but upon thrombin activation, there is insufficient platelet activation and restricted release function, accompanied by elevated ROS production and compromised mitochondrial functionality.

Key words: Platelets, Platelet Activation, ROS, Mitochondria

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