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

    作者

    Pang, YQ; Yang, J; Jia, CM; Zhang, R; Pang, Q

    作者单位

    [Pang, Yi-Qiang; Zhang, Rui; Pang, Qi] Shandong Univ, Shandong Prov Hosp, Cheeloo Coll Med, Dept Neurosurg, Jinan, Shandong, Peoples R China; [Pang, Yi-Qiang; Jia, Chun-Mei] Fourth Hosp Baotou, Dept Neurosurg, Baotou, Inner Mongolia, Peoples R China; [Yang, Jing] Baotou Med Coll, Dept Basic Med & Forens Med, Baotou, Inner Mongolia, Peoples R China

    摘要

    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-1 beta, 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.

    关键词

基本信息

  • 所属机构:

    归属医师: 庞琦 张睿

    PMID:34269215

    UT:000678125500036

    刊名:NEURAL REGENERATION RESEARCH

    年,卷(期):2022年17卷2期

    页码:395-

    DOI:10.4103/1673-5374.314317

    附件: other

    收录:   SCIE