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When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
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基础科学和病原发生学

Luis Pedro Bernardi1, Thomas Hugentobler Schlickmann1, Giovanna Carello-Collar2

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概括
此摘要是机器生成的。

介质干细胞衍生的细胞外囊泡 (MSC-EVs) 在缺血性中风 (IS) 的动物模型中始终调节微质反应,减少炎症并促进抗炎作用. 这些发现表明MSC-EVs可能有助于IS和阿尔茨海默病 (AD) 的恢复.

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科学领域:

  • 神经科学是一个神经科学.
  • 免疫学 免疫学 免疫学
  • 再生医学是一种再生医学.

背景情况:

  • 缺血性中风 (IS) 是阿尔茨海默病 (AD) 的已知危险因素.
  • 微质反应性与IS和AD有关,具有治疗点.
  • 之前的研究表明,介质干细胞衍生的细胞外囊泡 (MSC-EVs) 在IS模型中调节微质反应.

研究的目的:

  • 调查MSC-EVs对微质细胞的影响是否在IS早期和晚期之间有所不同.
  • 评估MSC-EVs对IS模型中促炎和抗炎微质标记物的影响.

主要方法:

  • 按照PRISMA 2020指南进行了系统的元分析,该协议在PROSPERO.上注册.
  • 在EMBASE,PubMed和Web of Science中搜索了IS动物模型中MSC-EVs治疗的研究.
  • 亚组分析使用随机效应模型对早期 (48-72小时) 和晚期 (≥168小时) IS阶段的MSC-EV影响进行了比较.

主要成果:

  • 在早期和晚期IS阶段,MSC-EV显著降低了促炎性标记物 (Iba1+,CD16+,CD32+,iNOS+).
  • 在早期和晚期IS阶段,MSC-EV显著增加了抗炎标志物 (Iba1+,Arg-1+,CD206+).
  • 这些影响在不同疾病阶段一致,表明持续的调制.

结论:

  • 在IS模型中,MSC-EV在降低促炎和增加抗炎微质反应方面表现出一致的有效性.
  • 在IS中,MSC-EVs对微质的调节作用是相独立的.
  • 这些发现支持MSC-EVs作为IS恢复和潜在的AD潜在的治疗策略.