• 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

铜离子螯合剂诱导脱髓鞘过程中的血脑屏障通透性。对免疫介导的脱髓鞘疾病发病机制的影响。

Blood-brain barrier permeability during Cuprizone-induced demyelination. Implications for the pathogenesis of immune-mediated demyelinating diseases.

作者信息

Bakker D A, Ludwin S K

出版信息

J Neurol Sci. 1987 Apr;78(2):125-37. doi: 10.1016/0022-510x(87)90055-4.

DOI:10.1016/0022-510x(87)90055-4
PMID:3553434
Abstract

Blood vessels in the superior cerebellar peduncles were studied in Cuprizone-fed mice for leakage of proteins into the parenchyma. The status of the blood-brain barrier was determined at various stages of demyelination both by tracer methods using horseradish peroxidase and immunochemically using antisera to extravasated serum proteins and was compared to three positive and negative control conditions. The results showed no evidence of significant protein leakage into the subendothelial basement membrane or extravascular space in Cuprizone mice, during the development of demyelination. The apparent lack of damage to the blood-brain barrier found in Cuprizone animals as compared to the blood-brain barrier alterations previously reported for immune-mediated demyelinating diseases, confirms the theory that these alterations are not a non-specific association of any demyelinating process, but are of primary pathogenetic importance in immune-mediated demyelination.

摘要

研究了用双环己酮草酰二腙喂养的小鼠小脑上脚中的血管,以检测蛋白质向实质内的渗漏情况。通过使用辣根过氧化物酶的示踪方法以及使用针对外渗血清蛋白的抗血清进行免疫化学方法,在脱髓鞘的各个阶段确定血脑屏障的状态,并将其与三种阳性和阴性对照情况进行比较。结果表明,在脱髓鞘发展过程中,双环己酮草酰二腙小鼠的内皮下基底膜或血管外间隙没有明显的蛋白质渗漏迹象。与先前报道的免疫介导的脱髓鞘疾病的血脑屏障改变相比,双环己酮草酰二腙动物中血脑屏障明显未受损伤,这证实了以下理论:这些改变不是任何脱髓鞘过程的非特异性关联,而是在免疫介导的脱髓鞘中具有主要的致病重要性。

相似文献

1
Blood-brain barrier permeability during Cuprizone-induced demyelination. Implications for the pathogenesis of immune-mediated demyelinating diseases.铜离子螯合剂诱导脱髓鞘过程中的血脑屏障通透性。对免疫介导的脱髓鞘疾病发病机制的影响。
J Neurol Sci. 1987 Apr;78(2):125-37. doi: 10.1016/0022-510x(87)90055-4.
2
Increased blood-brain barrier hyperpermeability coincides with mast cell activation early under cuprizone administration.在给予杯状蛋白后,血脑屏障通透性增加与肥大细胞活化同时发生。
PLoS One. 2020 Jun 8;15(6):e0234001. doi: 10.1371/journal.pone.0234001. eCollection 2020.
3
Blood-brain barrier hyperpermeability precedes demyelination in the cuprizone model.在 cuprizone 模型中,血脑屏障通透性增加先于脱髓鞘。
Acta Neuropathol Commun. 2017 Dec 1;5(1):94. doi: 10.1186/s40478-017-0497-6.
4
Age increases axon loss associated with primary demyelination in cuprizone-induced demyelination in C57BL/6 mice.在C57BL/6小鼠的铜螯合剂诱导的脱髓鞘模型中,年龄增加与原发性脱髓鞘相关的轴突损失。
J Neuroimmunol. 2006 Jun;175(1-2):69-76. doi: 10.1016/j.jneuroim.2006.03.002. Epub 2006 Apr 19.
5
Blood-brain barrier permeability to horseradish peroxidase in twitcher and cuprizone-intoxicated mice.
Brain Res. 1987 Nov 3;425(1):186-90. doi: 10.1016/0006-8993(87)90499-9.
6
Distribution of oligodendrocyte loss and mitochondrial toxicity in the cuprizone-induced experimental demyelination model.在氯化铜诱导的实验性脱髓鞘模型中少突胶质细胞丢失和线粒体毒性的分布。
J Neuroimmunol. 2013 Sep 15;262(1-2):128-31. doi: 10.1016/j.jneuroim.2013.06.012. Epub 2013 Jul 26.
7
Disparate Effects of Mesenchymal Stem Cells in Experimental Autoimmune Encephalomyelitis and Cuprizone-Induced Demyelination.间充质干细胞在实验性自身免疫性脑脊髓炎和铜螯合剂诱导的脱髓鞘中的不同作用。
PLoS One. 2015 Sep 25;10(9):e0139008. doi: 10.1371/journal.pone.0139008. eCollection 2015.
8
Localized Increased Permeability of Blood-Brain Barrier for Antibody Conjugates in the Cuprizone Model of Demyelination.在脱髓鞘的 Cuprizone 模型中,抗体缀合物的血脑屏障通透性增加。
Int J Mol Sci. 2023 Aug 11;24(16):12688. doi: 10.3390/ijms241612688.
9
TRPA1 deficiency is protective in cuprizone-induced demyelination-A new target against oligodendrocyte apoptosis.瞬时受体电位锚蛋白1缺乏在铜离子载体诱导的脱髓鞘中具有保护作用——一种针对少突胶质细胞凋亡的新靶点。
Glia. 2016 Dec;64(12):2166-2180. doi: 10.1002/glia.23051. Epub 2016 Aug 29.
10
Absence of CCL2 and CCL3 Ameliorates Central Nervous System Grey Matter But Not White Matter Demyelination in the Presence of an Intact Blood-Brain Barrier.在血脑屏障完整的情况下,CCL2 和 CCL3 的缺失可改善中枢神经系统灰质脱髓鞘,但不改善白质脱髓鞘。
Mol Neurobiol. 2016 Apr;53(3):1551-1564. doi: 10.1007/s12035-015-9113-6. Epub 2015 Feb 8.

引用本文的文献

1
Localized Increased Permeability of Blood-Brain Barrier for Antibody Conjugates in the Cuprizone Model of Demyelination.在脱髓鞘的 Cuprizone 模型中,抗体缀合物的血脑屏障通透性增加。
Int J Mol Sci. 2023 Aug 11;24(16):12688. doi: 10.3390/ijms241612688.
2
Animal models to investigate the effects of inflammation on remyelination in multiple sclerosis.用于研究炎症对多发性硬化症髓鞘再生影响的动物模型。
Front Mol Neurosci. 2022 Nov 3;15:995477. doi: 10.3389/fnmol.2022.995477. eCollection 2022.
3
Cuprizone feeding induces swollen astrocyte endfeet.
给予双硫仑喂养会导致星形胶质细胞足突肿胀。
Pflugers Arch. 2022 Dec;474(12):1275-1283. doi: 10.1007/s00424-022-02759-8. Epub 2022 Oct 15.
4
CAQK, a peptide associating with extracellular matrix components targets sites of demyelinating injuries.CAQK是一种与细胞外基质成分相关的肽,它靶向脱髓鞘损伤部位。
Front Cell Neurosci. 2022 Aug 22;16:908401. doi: 10.3389/fncel.2022.908401. eCollection 2022.
5
Nebivolol elicits a neuroprotective effect in the cuprizone model of multiple sclerosis in mice: emphasis on M1/M2 polarization and inhibition of NLRP3 inflammasome activation.比索洛尔在多发性硬化症的杯状胶模型中产生神经保护作用:重点关注 M1/M2 极化和抑制 NLRP3 炎性小体激活。
Inflammopharmacology. 2022 Dec;30(6):2197-2209. doi: 10.1007/s10787-022-01045-4. Epub 2022 Aug 10.
6
Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination.寡突胶质细胞死亡和髓鞘丢失在铜诱导模型中的作用:铜诱导脱髓鞘的内在和外在原因的最新综述。
Mol Neurodegener. 2022 May 7;17(1):34. doi: 10.1186/s13024-022-00538-8.
7
Neuroprotective effect of newly synthesized 4-aminopyridine derivatives on cuprizone-induced demyelination in mice-a behavioral and immunohistochemical study.新合成的 4-氨基吡啶衍生物对铜诱导的小鼠脱髓鞘的神经保护作用:行为学和免疫组织化学研究。
Amino Acids. 2021 Aug;53(8):1279-1286. doi: 10.1007/s00726-021-03035-2. Epub 2021 Jul 8.
8
Protective Effects of a Nano-Formulation of Curcumin against Cuprizone-Induced Demyelination in the Mouse Corpus Callosum.姜黄素纳米制剂对小鼠胼胝体中铜离子螯合剂诱导的脱髓鞘的保护作用。
Iran J Pharm Res. 2020 Summer;19(3):310-320. doi: 10.22037/ijpr.2020.112952.14033.
9
Increased blood-brain barrier hyperpermeability coincides with mast cell activation early under cuprizone administration.在给予杯状蛋白后,血脑屏障通透性增加与肥大细胞活化同时发生。
PLoS One. 2020 Jun 8;15(6):e0234001. doi: 10.1371/journal.pone.0234001. eCollection 2020.
10
Inflammation and Oxidative Stress in Multiple Sclerosis: Consequences for Therapy Development.多发性硬化症中的炎症与氧化应激:对治疗发展的影响
Oxid Med Cell Longev. 2020 May 12;2020:7191080. doi: 10.1155/2020/7191080. eCollection 2020.