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大鼠局灶纹状体卒中后胼胝体的炎症反应和继发性白质损伤。

Inflammatory Response and Secondary White Matter Damage to the Corpus Callosum after Focal Striatal Stroke in Rats.

机构信息

Laboratory of Functional and Structural Biology, Institute of Biological Sciences, Federal University of Pará (UFPA), Belém 66075-110, PA, Brazil.

Graduate Program in Health and Society, University of the State of Rio Grande do Norte (UERN), Mossoró 59610-210, RN, Brazil.

出版信息

Int J Mol Sci. 2022 Mar 16;23(6):3179. doi: 10.3390/ijms23063179.

DOI:10.3390/ijms23063179
PMID:35328600
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8955860/
Abstract

Stroke is one of the leading causes of death and long-term disabilities worldwide, resulting in a debilitating condition occasioned by disturbances in the cerebral vasculature. Primary damage due to metabolic collapse is a quick outcome following stroke, but a multitude of secondary events, including excitotoxicity, inflammatory response, and oxidative stress cause further cell death and functional impairment. In the present work, we investigated whether a primary ischemic damage into the dorsal striatum may cause secondary damage in the circumjacent corpus callosum (CC). Animals were injected with endothelin-1 and perfused at 3, 7, 14, and 30 post-lesion days (PLD). Sections were stained with Cresyl violet for basic histopathology and immunolabeled by antibodies against astrocytes (anti-GFAP), macrophages/microglia (anti-IBA1/anti MHC-II), oligodendrocytes (anti-TAU) and myelin (anti-MBP), and Anti-Nogo. There were conspicuous microgliosis and astrocytosis in the CC, followed by later oligodendrocyte death and myelin impairment. Our results suggest that secondary white matter damage in the CC follows a primary focal striatal ischemia in adult rats.

摘要

中风是全球范围内导致死亡和长期残疾的主要原因之一,会导致大脑血管紊乱引起的身体虚弱状况。代谢崩溃导致的原发性损伤是中风后的快速结果,但多种继发性事件,包括兴奋毒性、炎症反应和氧化应激,会导致进一步的细胞死亡和功能障碍。在本工作中,我们研究了背侧纹状体的原发性缺血损伤是否会导致周围胼胝体(CC)的继发性损伤。动物在注射内皮素-1后,在 3、7、14 和 30 天(PLD)进行灌注。用 Cresyl 紫进行基本组织病理学染色,并使用针对星形胶质细胞(抗 GFAP)、巨噬细胞/小胶质细胞(抗 IBA1/抗 MHC-II)、少突胶质细胞(抗 TAU)和髓鞘(抗 MBP)以及抗 Nogo 的抗体进行免疫标记。在 CC 中出现明显的小胶质细胞增生和星形胶质细胞增生,随后出现少突胶质细胞死亡和髓鞘损伤。我们的结果表明,成年大鼠的背侧纹状体局灶性缺血后会继发 CC 白质损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60d9/8955860/fdc98b7bae62/ijms-23-03179-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60d9/8955860/e0dc8368b9ea/ijms-23-03179-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60d9/8955860/fdc98b7bae62/ijms-23-03179-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60d9/8955860/e7731f3f4d5c/ijms-23-03179-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60d9/8955860/d3934f3f2481/ijms-23-03179-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60d9/8955860/0fcd914044ac/ijms-23-03179-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60d9/8955860/fdc98b7bae62/ijms-23-03179-g008.jpg

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