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脑出血后与质量效应相关的静水压力引起的神经损伤。

Neural Injuries Induced by Hydrostatic Pressure Associated With Mass Effect after Intracerebral Hemorrhage.

机构信息

Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400030, China.

Collaborative Innovation Center for Brain Science, Chongqing University, Chongqing, 400030, China.

出版信息

Sci Rep. 2018 Jun 15;8(1):9195. doi: 10.1038/s41598-018-27275-7.

DOI:10.1038/s41598-018-27275-7
PMID:29907795
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6003942/
Abstract

Mass effect induced by growing hematoma is one of the mechanisms by which intracerebral hemorrhage (ICH) may result in brain injuries. Our goal was to investigate the damage mechanism of hydrostatic pressure associated with mass effect and the cooperative effect of hydrostatic pressure plus hemoglobin on neural injuries. Loading hydrostatic pressure on neurons and injecting agarose gel in the right striatum of rats was performed to establish the in vitro and vivo ICH models, respectively. The elevated hydrostatic pressure associated with ICH suppressed neurons and neural tissues viability, and disturbed the axons and dendrites in vitro and vivo. Moreover, hydrostatic pressure could upregulate the expression of cleaved-caspase-3 and BAX, and downregulate Bcl-2 and Bcl-xL. Meanwhile, the toxicity of hemoglobin would be enhanced when conducted with hydrostatic pressure together. Furthermore, the exclusive hydrostatic pressure could upregulate the Piezo-2 expression, which reached a plateau at 8 h after ICH. And hemoglobin increased Piezo-2 expression significantly in vivo, and that was also promoted significantly by the elevated volume of Gel in the cooperative groups. Results indicated that hydrostatic pressure induced by mass effect not only gave rise to brain injuries directly, but also increased the toxicity of hemoglobin in the progress of secondary brain injury after ICH.

摘要

血肿增大引起的质量效应是脑出血（ICH）导致脑损伤的机制之一。我们的目标是研究与质量效应相关的静水压力损伤机制以及静水压力加血红蛋白对神经损伤的协同作用。通过对神经元施加静水压力并在大鼠右侧纹状体中注射琼脂糖凝胶，分别建立了体外和体内 ICH 模型。ICH 相关的升高的静水压力抑制神经元和神经组织的活力，并在体外和体内扰乱轴突和树突。此外，静水压力可上调裂解型 caspase-3 和 BAX 的表达，并下调 Bcl-2 和 Bcl-xL。同时，当与静水压力一起进行时，血红蛋白的毒性会增强。此外，单独的静水压力会增加 Piezo-2 的表达，ICH 后 8 小时达到平台期。血红蛋白在体内显著增加 Piezo-2 的表达，在协同组中凝胶体积增加也显著促进了 Piezo-2 的表达。结果表明，质量效应引起的静水压力不仅直接导致脑损伤，而且在 ICH 后继发性脑损伤过程中增加了血红蛋白的毒性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07bc/6003942/822290db2bab/41598_2018_27275_Fig10_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07bc/6003942/b7319dea0192/41598_2018_27275_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07bc/6003942/15c5c04a4e34/41598_2018_27275_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07bc/6003942/822290db2bab/41598_2018_27275_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07bc/6003942/c934291bc627/41598_2018_27275_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07bc/6003942/78b52d9e2746/41598_2018_27275_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07bc/6003942/055ea882caa7/41598_2018_27275_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07bc/6003942/44aec9fc39f6/41598_2018_27275_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07bc/6003942/d988e457f7ec/41598_2018_27275_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07bc/6003942/9505c5d3ff40/41598_2018_27275_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07bc/6003942/faa4e472c66a/41598_2018_27275_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07bc/6003942/b7319dea0192/41598_2018_27275_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07bc/6003942/15c5c04a4e34/41598_2018_27275_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07bc/6003942/822290db2bab/41598_2018_27275_Fig10_HTML.jpg

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