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缺氧预处理的骨髓间充质干细胞可保护神经元免受心脏骤停诱导的细胞焦亡。

Hypoxia-preconditioned bone marrow-derived mesenchymal stem cells protect neurons from cardiac arrest-induced pyroptosis.

作者信息

Tang Xiahong, Zheng Nan, Lin Qingming, You Yan, Gong Zheng, Zhuang Yangping, Wu Jiali, Wang Yu, Huang Hanlin, Ke Jun, Chen Feng

机构信息

Shengli Clinical Medical College of Fujian Medical University, Fujian Medical University, Fuzhou, Fujian Province, China.

Department of Emergency, Fujian Provincial Hospital, Fuzhou, Fujian Province, China.

出版信息

Neural Regen Res. 2025 Apr 1;20(4):1103-1123. doi: 10.4103/NRR.NRR-D-23-01922. Epub 2024 Jun 3.

DOI:10.4103/NRR.NRR-D-23-01922
PMID:38845218
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11438345/
Abstract

JOURNAL/nrgr/04.03/01300535-202504000-00027/figure1/v/2024-07-06T104127Z/r/image-tiff Cardiac arrest can lead to severe neurological impairment as a result of inflammation, mitochondrial dysfunction, and post-cardiopulmonary resuscitation neurological damage. Hypoxic preconditioning has been shown to improve migration and survival of bone marrow-derived mesenchymal stem cells and reduce pyroptosis after cardiac arrest, but the specific mechanisms by which hypoxia-preconditioned bone marrow-derived mesenchymal stem cells protect against brain injury after cardiac arrest are unknown. To this end, we established an in vitro co-culture model of bone marrow-derived mesenchymal stem cells and oxygen-glucose deprived primary neurons and found that hypoxic preconditioning enhanced the protective effect of bone marrow stromal stem cells against neuronal pyroptosis, possibly through inhibition of the MAPK and nuclear factor κB pathways. Subsequently, we transplanted hypoxia-preconditioned bone marrow-derived mesenchymal stem cells into the lateral ventricle after the return of spontaneous circulation in an 8-minute cardiac arrest rat model induced by asphyxia. The results showed that hypoxia-preconditioned bone marrow-derived mesenchymal stem cells significantly reduced cardiac arrest-induced neuronal pyroptosis, oxidative stress, and mitochondrial damage, whereas knockdown of the liver isoform of phosphofructokinase in bone marrow-derived mesenchymal stem cells inhibited these effects. To conclude, hypoxia-preconditioned bone marrow-derived mesenchymal stem cells offer a promising therapeutic approach for neuronal injury following cardiac arrest, and their beneficial effects are potentially associated with increased expression of the liver isoform of phosphofructokinase following hypoxic preconditioning.

摘要

《期刊》/nrgr/04.03/01300535 - 202504000 - 00027/图1/v/2024 - 07 - 06T104127Z/图像 - tiff 心脏骤停可因炎症、线粒体功能障碍和心肺复苏后神经损伤导致严重的神经功能障碍。缺氧预处理已被证明可改善骨髓间充质干细胞的迁移和存活，并减少心脏骤停后的细胞焦亡，但缺氧预处理的骨髓间充质干细胞预防心脏骤停后脑损伤的具体机制尚不清楚。为此，我们建立了骨髓间充质干细胞与氧 - 葡萄糖剥夺的原代神经元的体外共培养模型，发现缺氧预处理增强了骨髓基质干细胞对神经元焦亡的保护作用，可能是通过抑制丝裂原活化蛋白激酶和核因子κB途径。随后，我们将缺氧预处理的骨髓间充质干细胞移植到窒息诱导的8分钟心脏骤停大鼠模型自主循环恢复后的侧脑室。结果表明，缺氧预处理的骨髓间充质干细胞显著减少了心脏骤停诱导的神经元焦亡、氧化应激和线粒体损伤，而敲低骨髓间充质干细胞中磷酸果糖激酶的肝脏同工型则抑制了这些作用。总之，缺氧预处理的骨髓间充质干细胞为心脏骤停后神经元损伤提供了一种有前景的治疗方法，其有益作用可能与缺氧预处理后磷酸果糖激酶肝脏同工型表达增加有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d04/11438345/332cbcf96b87/NRR-20-1103-g010.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d04/11438345/c980fb1b7ede/NRR-20-1103-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d04/11438345/afb4c208a760/NRR-20-1103-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d04/11438345/332cbcf96b87/NRR-20-1103-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d04/11438345/f3e210991447/NRR-20-1103-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d04/11438345/aa2ce7c41947/NRR-20-1103-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d04/11438345/3293435cfaf9/NRR-20-1103-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d04/11438345/f019023759e1/NRR-20-1103-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d04/11438345/efe996f6ee55/NRR-20-1103-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d04/11438345/641e027cd544/NRR-20-1103-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d04/11438345/c980fb1b7ede/NRR-20-1103-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d04/11438345/afb4c208a760/NRR-20-1103-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d04/11438345/332cbcf96b87/NRR-20-1103-g010.jpg

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