中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2022, Vol. 17 ›› Issue (2): 395-400.doi: 10.4103/1673-5374.314317

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

低氧预适应减少NLRP3炎性小体保护脑缺血再灌注损伤 

  

  • 出版日期:2022-02-15 发布日期:2021-10-08

Hypoxic preconditioning reduces NLRP3 inflammasome expression and protects against cerebral ischemia/reperfusion injury

Yi-Qiang Pang1, 2, Jing Yang3, Chun-Mei Jia2, Rui Zhang1, Qi Pang1, *   

  1. 1Department of Neurosurgery, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong Province, China; 2Department of Neurosurgery, The Fourth Hospital of Baotou, Baotou, Inner Mongolia Autonomous Region, China; 3Department of Basic Medicine and Forensic Medicine, Baotou Medical College, Baotou, Inner Mongolia Autonomous Region, China 
  • Online:2022-02-15 Published:2021-10-08
  • Contact: Qi Pang, PhD, doctorpangqi@126.com.
  • Supported by:
    This work was supported by National Natural Science Foundation of China, No. 81771270 (to QP); Inner Mongolia Science Foundation of China, No. 2020MS08063 (to YQP); Health and Family Planning Scientific Research Plan Project of Inner Mongolia Autonomous Region of China, No. 201702138 (to YQP); Baotou Science and Technology Plan Project of China, No. 2018C2007-4-10 (to YQP); Baotou Medical and Health Science and Technology Project of China, No. wsjj2019036 (to JY); and Baotou Medical College Foundation of China, No. BSJJ201904 (to JY).

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摘要：

低氧预适应能够预防脑缺血再灌注损伤，但其潜在机制仍不明确。为此，实验设计首先对小鼠进行连续间歇低氧预适应，1h后以大脑中动脉闭塞再灌注方法建立脑缺血再灌注损伤模型。见脑缺血再灌注损伤小鼠Bederson神经功能评分上调，脑梗死体积明显增加，海马病理损伤明显，细胞凋亡明显增加，脑组织白细胞介素1β、白细胞介素6和白细胞介素8水平上调，脑组织NLRP3炎症小体相关蛋白caspase-1，消皮素D和NLRP3的表达增加，而经低氧预适应干预则能显著抑制上述现象。实验结果说明，低氧预适应通过降低NLRP3炎症小体的表达减轻了小鼠大脑缺血再灌注损伤。实验于2019年11月经包头市第四医院医学伦理委员会批准（批准号DWLL2019001）。

https://orcid.org/0000-0001-5368-8417 (Qi Pang)

关键词: 低氧预适应, 脑缺血再灌注损伤, 海马, 细胞死亡, 细胞凋亡, NLRP3炎性小体, caspase-1, 消皮素D

Abstract: Hypoxic preconditioning can protect against cerebral ischemia/reperfusion injury. However, the underlying mechanisms that mediate this effect are not completely clear. In this study, mice were pretreated with continuous, intermittent hypoxic preconditioning; 1 hour later, cerebral ischemia/reperfusion models were generated by middle cerebral artery occlusion and reperfusion. Compared with control mice, mice with cerebral ischemia/reperfusion injury showed increased Bederson neurological function scores, significantly increased cerebral infarction volume, obvious pathological damage to the hippocampus, significantly increased apoptosis; upregulated interleukin-1β, interleukin-6, and interleukin-8 levels in brain tissue; and increased expression levels of NOD-like receptor family pyrin domain containing 3 (NLRP3), NLRP inflammasome-related protein caspase-1, and gasdermin D. However, hypoxic preconditioning significantly inhibited the above phenomena. Taken together, these data suggest that hypoxic preconditioning mitigates cerebral ischemia/reperfusion injury in mice by reducing NLRP3 inflammasome expression. This study was approved by the Medical Ethics Committee of the Fourth Hospital of Baotou, China (approval No. DWLL2019001) in November 2019.

Key words: apoptosis, caspase-1, cell death, cerebral ischemia/reperfusion injury, gasdermin D, hippocampus, hypoxic preconditioning, NLRP3 inflammasome

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