• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

慢性脑灌注不足诱导大鼠脑内胶质细胞激活及白质改变:一项免疫组织化学研究

Glial activation and white matter changes in the rat brain induced by chronic cerebral hypoperfusion: an immunohistochemical study.

作者信息

Wakita H, Tomimoto H, Akiguchi I, Kimura J

机构信息

Department of Neurology, Kyoto University, Faculty of Medicine, Japan.

出版信息

Acta Neuropathol. 1994;87(5):484-92. doi: 10.1007/BF00294175.

DOI:10.1007/BF00294175
PMID:8059601
Abstract

Activation of glial cells and white matter changes (rarefaction of the white matter) induced in the rat brain by permanent bilateral occlusion of the common carotid arteries were immunohistochemically investigated up to 90 days. One day after ligation of the arteries, expression of the major histocompatibility complex (MHC) class I antigen in microglia increased in the white matter including the optic nerve, optic tract, corpus callosum, internal capsule, anterior commissure and traversing fiber bundles of the caudoputamen. After 3 days of occlusion, MHC class I antigen was still elevated and in addition MHC class II antigen and leukocyte common antigen were up-regulated in the microglia in these same regions. Astroglia, labeled with glial fibrillary acidic protein, increased in number in these regions after 7 days of occlusion. A few lymphocytes, labeled with CD4 or CD8 antibodies, were scattered in the neural parenchyma 1 h after occlusion. Activation of glial cells and infiltration of lymphocytes persisted after 90 days of occlusion in the white matter and the retinofugal pathway. However, cellular activation and infiltration in microinfarcts of the gray matter was less extensive and was substantially diminished 30 days after occlusion. The white matter changes were most intense in the optic nerve and optic tract, moderate in the medial part of the corpus callosum, internal capsule and anterior commissure, and slight in the fiber bundles of the caudoputamen. These results indicated that chronic cerebral hypoperfusion induced glial activation preferentially in the white matter. This activation seemed to be an early indicator of the subsequent changes in the white matter.

摘要

通过永久性双侧颈总动脉闭塞诱导大鼠脑内胶质细胞激活和白质变化(白质稀疏),采用免疫组织化学方法对其进行了长达90天的研究。动脉结扎后1天,包括视神经、视束、胼胝体、内囊、前连合和尾壳核穿行纤维束在内的白质中,小胶质细胞主要组织相容性复合体(MHC)I类抗原的表达增加。闭塞3天后,MHC I类抗原仍升高,此外,这些相同区域的小胶质细胞中MHC II类抗原和白细胞共同抗原上调。用胶质纤维酸性蛋白标记的星形胶质细胞在闭塞7天后在这些区域数量增加。闭塞1小时后,少数用CD4或CD8抗体标记的淋巴细胞散在于神经实质中。闭塞90天后,白质和视网膜神经通路中胶质细胞的激活和淋巴细胞浸润持续存在。然而,灰质微梗死中的细胞激活和浸润程度较轻,闭塞30天后明显减轻。白质变化在视神经和视束中最为明显,在胼胝体、内囊和前连合的内侧部分中等程度,在尾壳核的纤维束中轻微。这些结果表明,慢性脑灌注不足优先诱导白质中的胶质细胞激活。这种激活似乎是白质后续变化的早期指标。

相似文献

1
Glial activation and white matter changes in the rat brain induced by chronic cerebral hypoperfusion: an immunohistochemical study.慢性脑灌注不足诱导大鼠脑内胶质细胞激活及白质改变:一项免疫组织化学研究
Acta Neuropathol. 1994;87(5):484-92. doi: 10.1007/BF00294175.
2
Protective effect of cyclosporin A on white matter changes in the rat brain after chronic cerebral hypoperfusion.环孢素A对慢性脑灌注不足大鼠脑白质变化的保护作用。
Stroke. 1995 Aug;26(8):1415-22. doi: 10.1161/01.str.26.8.1415.
3
Dose-dependent, protective effect of FK506 against white matter changes in the rat brain after chronic cerebral ischemia.
Brain Res. 1998 May 4;792(1):105-13. doi: 10.1016/s0006-8993(98)00126-7.
4
Axonal damage and demyelination in the white matter after chronic cerebral hypoperfusion in the rat.大鼠慢性脑灌注不足后白质中的轴突损伤和脱髓鞘
Brain Res. 2002 Jan 4;924(1):63-70. doi: 10.1016/s0006-8993(01)03223-1.
5
Experimental cerebral hypoperfusion induces white matter injury and microglial activation in the rat brain.实验性脑灌注不足可导致大鼠脑白质损伤和小胶质细胞激活。
Acta Neuropathol. 2004 Jul;108(1):57-64. doi: 10.1007/s00401-004-0864-9. Epub 2004 May 8.
6
[Changes in glial cells in Binswanger-type infarction].
No To Shinkei. 1994 Aug;46(8):771-9.
7
Caudoputamen is damaged by hypocapnia during mechanical ventilation in a rat model of chronic cerebral hypoperfusion.在慢性脑灌注不足大鼠模型中,机械通气期间低碳酸血症会损伤尾壳核。
Stroke. 2001 Dec 1;32(12):2920-5. doi: 10.1161/hs1201.100216.
8
Diazoxide and dimethyl sulphoxide alleviate experimental cerebral hypoperfusion-induced white matter injury in the rat brain.二氮嗪和二甲基亚砜可减轻实验性脑灌注不足诱导的大鼠脑白质损伤。
Neurosci Lett. 2005 Jan 20;373(3):195-9. doi: 10.1016/j.neulet.2004.10.007. Epub 2004 Oct 27.
9
Neuroprotection by cilostazol, a phosphodiesterase type 3 inhibitor, against apoptotic white matter changes in rat after chronic cerebral hypoperfusion.西洛他唑(一种磷酸二酯酶3抑制剂)对慢性脑灌注不足大鼠凋亡性白质变化的神经保护作用。
Brain Res. 2006 Apr 12;1082(1):182-91. doi: 10.1016/j.brainres.2006.01.088. Epub 2006 Mar 3.
10
[White matter lesions after occlusion of the bilateral carotid arteries in the rat--temporal profile of cerebral blood flow (CBF), oligodendroglia and myelin].[大鼠双侧颈动脉闭塞后的白质病变——脑血流(CBF)、少突胶质细胞和髓鞘的时间变化]
No To Shinkei. 1997 Jul;49(7):639-44.

引用本文的文献

1
Engineered endoplasmic reticulum-targeting nanodrugs with Piezo1 inhibition and promotion of cell uptake for subarachnoid hemorrhage inflammation repair.具有Piezo1抑制作用并促进细胞摄取以用于蛛网膜下腔出血炎症修复的工程化内质网靶向纳米药物。
J Nanobiotechnology. 2025 Apr 5;23(1):274. doi: 10.1186/s12951-025-03305-1.
2
Acupuncture Improves Chronic Cerebral Ischemia by Inhibiting the CKLF1/HIF-1α/VEGF/Notch1 Signaling Pathway.针刺通过抑制CKLF1/HIF-1α/VEGF/Notch1信号通路改善慢性脑缺血
CNS Neurosci Ther. 2025 Mar;31(3):e70246. doi: 10.1111/cns.70246.
3
The pathogenesis of cerebral small vessel disease and vascular cognitive impairment.

本文引用的文献

1
Ischemic infarction and swelling in the rat brain.
Arch Pathol. 1960 May;69:544-53.
2
NEUROPATHOLOGICAL CHANGES LATE IN CEREBRAL EDEMA: THE RELATIONSHIP TO TRAUMA, HYPERTENSIVE DISEASE AND BINSWANGER'S ENCEPHALOPATHY.脑水肿后期的神经病理学改变:与创伤、高血压病及宾斯旺格脑病的关系
J Neuropathol Exp Neurol. 1963 Jul;22:500-11. doi: 10.1097/00005072-196307000-00011.
3
The relationship between edema, blood-brain-barrier and tissue elements in a local brain injury.局部脑损伤中水肿、血脑屏障与组织成分之间的关系。
脑小血管病与血管性认知障碍的发病机制。
Physiol Rev. 2025 Jul 1;105(3):1075-1171. doi: 10.1152/physrev.00028.2024. Epub 2025 Feb 18.
4
Oxidative stress and chronic cerebral hypoperfusion: An overview from preclinical rodent models.氧化应激与慢性脑灌注不足:来自临床前啮齿动物模型的概述
J Cereb Blood Flow Metab. 2025 Mar;45(3):381-395. doi: 10.1177/0271678X241305899. Epub 2024 Dec 12.
5
Cerebral hypoperfusion reduces tau accumulation.脑灌注不足可减少tau蛋白积累。
Ann Clin Transl Neurol. 2025 Jan;12(1):69-85. doi: 10.1002/acn3.52247. Epub 2024 Dec 2.
6
Treatment of vascular dementia in female rats with AV-001, an Angiopoietin-1 mimetic peptide, improves cognitive function.用血管生成素-1模拟肽AV-001治疗雌性大鼠血管性痴呆可改善认知功能。
Front Neurosci. 2024 Jul 10;18:1408205. doi: 10.3389/fnins.2024.1408205. eCollection 2024.
7
Dental pulp mesenchymal stem cell-derived exosomes inhibit neuroinflammation and microglial pyroptosis in subarachnoid hemorrhage via the miRNA-197-3p/FOXO3 axis.牙髓间充质干细胞来源的外泌体通过 miRNA-197-3p/FOXO3 轴抑制蛛网膜下腔出血中的神经炎症和小胶质细胞焦亡。
J Nanobiotechnology. 2024 Jul 19;22(1):426. doi: 10.1186/s12951-024-02708-w.
8
Dexmedetomidine Inhibits Hippocampal Neuronal Damage Caused by Persistent Isoflurane-Induced Hypotension in Rat Model of Chronic Cerebral Hypoperfusion.右美托咪定抑制慢性脑灌注不足大鼠模型中由持续异氟烷诱导的低血压所引起的海马神经元损伤。
Cureus. 2024 Jun 2;16(6):e61522. doi: 10.7759/cureus.61522. eCollection 2024 Jun.
9
Hope for vascular cognitive impairment: Ac-YVAD-cmk as a novel treatment against white matter rarefaction.血管性认知障碍的希望:Ac-YVAD-cmk 作为一种治疗脑白质疏松症的新方法。
PLoS One. 2024 Apr 17;19(4):e0299703. doi: 10.1371/journal.pone.0299703. eCollection 2024.
10
Inhibition of Glial Activation and Subsequent Reduction in White Matter Damage through Supplementation with a Combined Extract of Wheat Bran, Citrus Peel, and Jujube in a Rat Model of Vascular Dementia.在血管性痴呆大鼠模型中,通过补充麦麸、柑橘皮和枣的联合提取物抑制胶质细胞活化并随后减少白质损伤。
Curr Issues Mol Biol. 2024 Feb 11;46(2):1485-1502. doi: 10.3390/cimb46020096.
J Neuropathol Exp Neurol. 1958 Oct;17(4):548-64. doi: 10.1097/00005072-195810000-00002.
4
T-cell infiltration and expression of MHC class II antigen by macrophages and microglia in a heterogeneous group in leukoencephalopathy.白细胞脑病异质性群体中T细胞浸润以及巨噬细胞和小胶质细胞MHC II类抗原的表达。
Am J Pathol. 1993 Aug;143(2):579-86.
5
Changes in local cerebral blood flow following bilateral carotid occlusion in spontaneously hypertensive and normotensive rats.
Stroke. 1981 Nov-Dec;12(6):874-6. doi: 10.1161/01.str.12.6.874.
6
Temporal profile of neuronal damage in a model of transient forebrain ischemia.短暂性前脑缺血模型中神经元损伤的时间进程
Ann Neurol. 1982 May;11(5):491-8. doi: 10.1002/ana.410110509.
7
Delayed neuronal death in the gerbil hippocampus following ischemia.沙土鼠海马缺血后迟发性神经元死亡
Brain Res. 1982 May 6;239(1):57-69. doi: 10.1016/0006-8993(82)90833-2.
8
Experimental bilateral carotid artery occlusion: a study of the optic nerve in the rat.实验性双侧颈动脉闭塞:大鼠视神经的研究
Neuropathol Appl Neurobiol. 1984 Nov-Dec;10(6):423-8. doi: 10.1111/j.1365-2990.1984.tb00391.x.
9
An experimental model of carotid artery occlusive disease.颈动脉闭塞性疾病的实验模型。
Am J Ophthalmol. 1984 Feb;97(2):168-72. doi: 10.1016/s0002-9394(14)76086-6.
10
Effects of cerebral ischemia in various strains of rats.
Proc Soc Exp Biol Med. 1965 Oct;120(1):208-9. doi: 10.3181/00379727-120-30487.