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过表达Sox2的神经干细胞可缓解出血后脑积水的脑室扩大和神经功能障碍。

Sox2-overexpressing neural stem cells alleviate ventricular enlargement and neurological dysfunction in posthemorrhagic hydrocephalus.

作者信息

Gao Baocheng, Wang Haoxiang, Hu Shuang, Zhong Kunhong, Liu Xiaoyin, Deng Ziang, Li Yuanyou, Tong Aiping, Zhou Liangxue

机构信息

Department of Neurosurgery, West China Medical School, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.

Department of Neurosurgery, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming, Yunnan Province, China.

出版信息

Neural Regen Res. 2026 Feb 1;21(2):769-779. doi: 10.4103/NRR.NRR-D-24-01491. Epub 2025 Apr 30.

DOI:10.4103/NRR.NRR-D-24-01491
PMID:40326987
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12220719/
Abstract

JOURNAL/nrgr/04.03/01300535-202602000-00045/figure1/v/2025-05-05T160104Z/r/image-tiff Neural stem cells (NSCs) have the potential for self-renewal and multidirectional differentiation, and their transplantation has achieved good efficacy in a variety of diseases. However, only 1%-10% of transplanted NSCs survive in the ischemic and hypoxic microenvironment of posthemorrhagic hydrocephalus. Sox2 is an important factor for NSCs to maintain proliferation. Therefore, Sox2-overexpressing NSCs (NSCSox2) may be more successful in improving neurological dysfunction after posthemorrhagic hydrocephalus. In this study, human NSCSox2 was transplanted into a posthemorrhagic hydrocephalus mouse model, and retinoic acid was administered to further promote NSC differentiation. The results showed that NSCSox2 attenuated the ventricular enlargement caused by posthemorrhagic hydrocephalus and improved neurological function. NSCSox2 also promoted nerve regeneration, inhibited neuroinflammation and promoted M2 polarization (anti-inflammatory phenotype), thereby reducing cerebrospinal fluid secretion in choroid plexus. These findings suggest that NSCSox2 rescued ventricular enlargement and neurological dysfunction induced by posthemorrhagic hydrocephalus through neural regeneration and modulation of inflammation.

摘要

《期刊》/nrgr/04.03/01300535 - 202602000 - 00045/图1/v/2025 - 05 - 05T160104Z/图像 - 标签图像文件格式 神经干细胞（NSCs）具有自我更新和多向分化的潜力，并且它们的移植在多种疾病中已取得良好疗效。然而，在出血后脑积水的缺血缺氧微环境中，只有1% - 10%的移植神经干细胞存活。Sox2是神经干细胞维持增殖的重要因素。因此，过表达Sox2的神经干细胞（NSCSox2）在改善出血后脑积水后的神经功能障碍方面可能更成功。在本研究中，将人NSCSox2移植到出血后脑积水小鼠模型中，并给予视黄酸以进一步促进神经干细胞分化。结果表明，NSCSox2减轻了出血后脑积水引起的脑室扩大并改善了神经功能。NSCSox2还促进神经再生，抑制神经炎症并促进M2极化（抗炎表型），从而减少脉络丛中的脑脊液分泌。这些发现表明，NSCSox2通过神经再生和炎症调节挽救了出血后脑积水诱导的脑室扩大和神经功能障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a51/12220719/f19b612ddc55/NRR-21-769-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a51/12220719/72362d47462b/NRR-21-769-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a51/12220719/781550d7223a/NRR-21-769-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a51/12220719/8b94198e9f03/NRR-21-769-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a51/12220719/f19b612ddc55/NRR-21-769-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a51/12220719/72362d47462b/NRR-21-769-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a51/12220719/c968b770d120/NRR-21-769-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a51/12220719/1bfaeeba5d90/NRR-21-769-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a51/12220719/80ae6d9c827a/NRR-21-769-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a51/12220719/781550d7223a/NRR-21-769-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a51/12220719/8b94198e9f03/NRR-21-769-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a51/12220719/f19b612ddc55/NRR-21-769-g009.jpg

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本文引用的文献

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Cerebrospinal fluid efflux through dynamic paracellular pores on venules as a missing piece of the brain drainage system.脑脊液通过小静脉上动态的细胞旁孔流出，这是脑引流系统中缺失的一环。
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