中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2025, Vol. 20 ›› Issue (8): 2199-2217.doi: 10.4103/NRR.NRR-D-23-01985

• 综述:神经损伤修复保护与再生 • 上一篇    下一篇

缺血性脑卒中后神经发生的增强：探索内源性和外源性干细胞之间的相互作用

  

  • 出版日期:2025-08-15 发布日期:2024-12-12

Neuroprotective potential for mitigating ischemiareperfusion-induced damage

Zi Ye1, #, Runqing Liu1, #, Hangxing Wang2 , Aizhen Zuo1 , Cen Jin3 , Nan Wang4 , Huiqi Sun5 , Luqian Feng6 , Hua Yang6, *   

  1. 1 The Clinical Medical College, Guizhou Medical University, Guiyang, Guizhou Province, China;  2 Division of Infectious Diseases, Department of Internal Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China;  3 School of Medical Imaging, Guizhou Medical University, Guiyang, Guizhou Province, China;  4 Division of Gastroenterology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China;  5 The Second Clinical Medical College, Lanzhou University, Lanzhou, Gansu Province, China;  6 Department of Neurosurgery, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province, China
  • Online:2025-08-15 Published:2024-12-12
  • Contact: Hua Yang, MD, yhmed@163.com

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摘要：

脑缺血后的再灌注会对脑组织的结构和功能造成损害，加重患者的病情，这种现象被称为脑缺血再灌注损伤。目前的研究已经阐明了Sirtuin蛋白家族（Sirtuins，SIRTs）在调节脑脑缺血再灌注损伤中的神经保护作用。然而，将其作为一种新的干预靶点来影响脑脑缺血再灌注损伤预后的潜力还需要进一步探索。鉴于此，文章概述了SIRTs的起源和研究进展，重点讨论了SIRTs参与影响脑缺血再灌注损伤的各种机制，包括炎症、氧化应激、血脑屏障损伤、细胞凋亡、热蛋白沉积和自噬。通过调节SIRTs的表达并影响核转录因子κB信号传导、单磷酸腺苷激活蛋白激酶（AMPK）和叉头盒O（FoxO）参与的氧化应激等代表性通路，探索与SIRTs相关的治疗途径，从而改善脑缺血再灌注损伤的预后。文章还总结了调节SIRTs表达的内源性物质（如RNA和激素）、药物、膳食补充剂和新兴疗法的潜力，并发现调节SIRTs在与其他风险因素相结合时也能减轻脑脑缺血再灌注损伤。虽然SIRTs有希望成为治疗脑脑缺血再灌注损伤的潜在靶点，但目前的研究大多基于啮齿类动物模型，这与人类的昼夜节律相反，可能会影响以SIRTs为靶点的药物疗法的疗效。总之，这篇综述为SIRTs在脑脑缺血再灌注损伤的病理和治疗中的作用提供了新的见解。

https://orcid.org/0000-0002-3473-8498 (Hua Yang)

关键词: 细胞凋亡, 自噬, 血脑屏障, 饮食补充剂, 药物, 激素, 炎症, 神经保护, 氧化应激, 预后, 焦亡, 再灌注损伤, 风险因素, RNA, 疗法

Abstract: Reperfusion following cerebral ischemia causes both structural and functional damage to brain tissue and could aggravate a patient’s condition; this phenomenon is known as cerebral ischemia-reperfusion injury. Current studies have elucidated the neuroprotective role of the sirtuin protein family (Sirtuins) in modulating cerebral ischemia-reperfusion injury. However, the potential of utilizing it as a novel intervention target to influence the prognosis of cerebral ischemia-reperfusion injury requires additional exploration. In this review, the origin and research progress of Sirtuins are summarized, suggesting the involvement of Sirtuins in diverse mechanisms that affect cerebral ischemia-reperfusion injury, including inflammation, oxidative stress, blood–brain barrier damage, apoptosis, pyroptosis, and autophagy. The therapeutic avenues related to Sirtuins that may improve the prognosis of cerebral ischemia-reperfusion injury were also investigated by modulating Sirtuins expression and affecting representative pathways, such as nuclear factor-kappa B signaling, oxidative stress mediated by adenosine monophosphate-activated protein kinase, and the forkhead box O. This review also summarizes the potential of endogenous substances, such as RNA and hormones, drugs, dietary supplements, and emerging therapies that regulate Sirtuins expression. This review also reveals that regulating Sirtuins mitigates cerebral ischemia-reperfusion injury when combined with other risk factors. While Sirtuins show promise as a potential target for the treatment of cerebral ischemiareperfusion injury, most recent studies are based on rodent models with circadian rhythms that are distinct from those of humans, potentially influencing the efficacy of Sirtuinstargeting drug therapies. Overall, this review provides new insights into the role of Sirtuins in the pathology and treatment of cerebral ischemia-reperfusion injury.

Key words: apoptosis, autophagy, blood–brain barrier, dietary supplements, drug, hormones, inflammation, neuroprotection, oxidative stress, prognosis, pyroptosis, reperfusion injury, risk factors, RNA, therapeutics