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血管生成素2的神经保护作用与缺血性脑卒中后小鼠脑内血管生成相关。

Neuroprotective Effect of Angiopoietin2 Is Associated with Angiogenesis in Mouse Brain Following Ischemic Stroke.

作者信息

Lv Ling-Ling, Du Yi-Ting, Chen Xiao, Lei Yu, Sun Feng-Yan

机构信息

Department of Neurobiology and State Key Laboratory of Medical Neurobiology, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai 200032, China.

Institute for Basic Research on Aging and Medicine of School of Basic Medical Sciences and National Clinical Research Center for Aging and Medicine, Huashan Hospital, Hanghai Medical College, Fudan University, Shanghai 200032, China.

出版信息

Brain Sci. 2022 Oct 24;12(11):1428. doi: 10.3390/brainsci12111428.

DOI:10.3390/brainsci12111428
PMID:36358355
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9688484/
Abstract

Angiogenic factors play an important role in protecting, repairing, and reconstructing vessels after ischemic stroke. In the brains of transient focal cerebral ischemic mice, we observed a reduction in infarct volume after the administration of Angiopoietin 2 (Angpt2), but whether this process is promoted by Angpt2-induced angiogenesis has not been fully elaborated. Therefore, this study explored the angiogenic activities, in reference to CD34 which is a marker of activated ECs and blood vessels, of cultured ECs in vitro and in ischemic damaged cerebral area in mice following Angpt2 administration. Our results demonstrate that Angpt2 administration (100 ng/mL) is neuroprotective by significantly increasing the CD34 expression in in vitro-cultured ECs, reducing the infarct volume and mitigating neuronal loss, as well as enhancing CD34 vascular length and area. In conclusion, these results indicate that Angpt2 promotes repair and attenuates ischemic injury, and that the mechanism of this is closely associated with angiogenesis in the brain after stroke.

摘要

血管生成因子在缺血性中风后血管的保护、修复和重建中发挥着重要作用。在短暂性局灶性脑缺血小鼠的大脑中,我们观察到给予血管生成素2(Angpt2)后梗死体积减小,但这一过程是否由Angpt2诱导的血管生成所促进尚未完全阐明。因此,本研究参照作为活化内皮细胞和血管标志物的CD34,探讨了给予Angpt2后体外培养的内皮细胞以及小鼠缺血损伤脑区的血管生成活性。我们的结果表明,给予Angpt2(100 ng/mL)具有神经保护作用,可显著增加体外培养的内皮细胞中CD34的表达,减小梗死体积并减轻神经元损失,同时增加CD34血管长度和面积。总之,这些结果表明Angpt2促进修复并减轻缺血性损伤,其机制与中风后脑内血管生成密切相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7124/9688484/265f205bcf48/brainsci-12-01428-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7124/9688484/47e27f66bf52/brainsci-12-01428-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7124/9688484/265f205bcf48/brainsci-12-01428-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7124/9688484/47e27f66bf52/brainsci-12-01428-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7124/9688484/265f205bcf48/brainsci-12-01428-g002.jpg

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