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中华危重症医学杂志(电子版) ›› 2023, Vol. 16 ›› Issue (03) : 240 -244. doi: 10.3877/cma.j.issn.1674-6880.2023.03.012

综述

细胞焦亡在脓毒症相关性脑病中的作用研究进展
周爽, 赵敏()   
  1. 110004 沈阳,中国医科大学附属盛京医院急诊科
  • 收稿日期:2022-10-18 出版日期:2023-06-30
  • 通信作者: 赵敏
  • 基金资助:
    辽宁省自然科学基金项目(201602879)
  • Received:2022-10-18 Published:2023-06-30
引用本文:

周爽, 赵敏. 细胞焦亡在脓毒症相关性脑病中的作用研究进展[J]. 中华危重症医学杂志(电子版), 2023, 16(03): 240-244.

脓毒症是由于宿主对感染的反应失调而导致的危及生命的器官功能障碍[1]。机体各部分的感染均可引起脓毒症,其病死率高,预后差。脓毒症相关性脑病(sepsis-associated encephalopathy,SAE)是脓毒症急性期和预后期最常见的并发症之一,有高达70%的脓毒症患者最终会发展到SAE[2]。它是由于宿主反应失调且中枢神经系统没有直接感染、结构异常或其他类型脑病的证据而导致的弥漫性脑功能障碍[3]。在达到脓毒症诊断标准之前,SAE的症状可能已经存在,急性期的症状从精神、行为的改变到昏迷,后期甚至会存在长期的认知障碍[3-4]。SAE的病理生理及潜在分子机制尚未完全阐明,但大多数学者认为SAE的病因是多因素的,可能有多种病理机制共同参与、互相影响,在不同程度上促进了SAE的发展。这些因素包括缺血或出血损伤、血脑屏障破坏、脑微循环异常、脑代谢异常(包括氧化应激、线粒体功能障碍等)、大量炎症因子释放、神经递质功能紊乱等[5]。探索SAE更多的治疗方式及分子机制,具有重要的临床意义。目前,细胞焦亡被认为可能参与了SAE的病理过程,抑制细胞焦亡有利于降低炎症级联反应,减轻SAE造成的脑损伤。因此,本研究将对脓毒症细胞焦亡在SAE中的作用研究进展进行综述。

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