Neural Regeneration Research ›› 2022, Vol. 17 ›› Issue (2): 395-400.doi: 10.4103/1673-5374.314317

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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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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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