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本文引用的文献

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The "inflammatory penumbra" in ischemic stroke: From clinical data to experimental evidence.缺血性卒中的“炎症半暗带”:从临床数据到实验证据
Eur Stroke J. 2016 Mar;1(1):20-27. doi: 10.1177/2396987316630249. Epub 2016 Mar 1.
2
Brain regulatory T cells suppress astrogliosis and potentiate neurological recovery.脑调节性 T 细胞抑制星形胶质细胞增生并增强神经功能恢复。
Nature. 2019 Jan;565(7738):246-250. doi: 10.1038/s41586-018-0824-5. Epub 2019 Jan 2.
3
Serotonin Selective Reuptake Inhibitors (SSRIs) and Stroke.选择性 5-羟色胺再摄取抑制剂(SSRIs)与卒中。
Curr Neurol Neurosci Rep. 2018 Oct 23;18(12):100. doi: 10.1007/s11910-018-0904-9.
4
Probiotics importance and their immunomodulatory properties.益生菌的重要性及其免疫调节特性。
J Cell Physiol. 2019 Jun;234(6):8008-8018. doi: 10.1002/jcp.27559. Epub 2018 Oct 14.
5
Sphingosine 1-phosphate receptor subtype 3 (S1P) contributes to brain injury after transient focal cerebral ischemia via modulating microglial activation and their M1 polarization.鞘氨醇 1-磷酸受体亚型 3(S1P)通过调节小胶质细胞的激活及其 M1 极化,参与短暂性局灶性脑缺血后的脑损伤。
J Neuroinflammation. 2018 Oct 10;15(1):284. doi: 10.1186/s12974-018-1323-1.
6
Roles of Specialized Pro-Resolving Lipid Mediators in Cerebral Ischemia Reperfusion Injury.特殊促消退脂质介质在脑缺血再灌注损伤中的作用
Front Neurol. 2018 Jul 31;9:617. doi: 10.3389/fneur.2018.00617. eCollection 2018.
7
Experimental ischemic stroke induces long-term T cell activation in the brain.实验性缺血性脑卒中诱导大脑中长期的 T 细胞激活。
J Cereb Blood Flow Metab. 2019 Nov;39(11):2268-2276. doi: 10.1177/0271678X18792372. Epub 2018 Aug 10.
8
Anti-inflammatory treatments for stroke: from bench to bedside.中风的抗炎治疗:从实验台到临床应用
Ther Adv Neurol Disord. 2018 Jul 30;11:1756286418789854. doi: 10.1177/1756286418789854. eCollection 2018.
9
CK2 inhibition confers functional protection to young and aging axons against ischemia by differentially regulating the CDK5 and AKT signaling pathways.CK2 抑制通过差异化调节 CDK5 和 AKT 信号通路,为年轻和衰老的轴突提供针对缺血的功能保护。
Neurobiol Dis. 2019 Jun;126:47-61. doi: 10.1016/j.nbd.2018.05.011. Epub 2018 Jun 23.
10
The gut microbiome primes a cerebroprotective immune response after stroke.肠道微生物组在中风后引发脑保护性免疫反应。
J Cereb Blood Flow Metab. 2018 Aug;38(8):1293-1298. doi: 10.1177/0271678X18780130. Epub 2018 May 30.

动物模型和人类中风后的重塑过程。

Post-stroke remodeling processes in animal models and humans.

机构信息

Toulouse NeuroImaging Center (ToNIC), INSERM, University Paul Sabatier, UPS, Toulouse, France.

出版信息

J Cereb Blood Flow Metab. 2020 Jan;40(1):3-22. doi: 10.1177/0271678X19882788. Epub 2019 Oct 23.

DOI:10.1177/0271678X19882788
PMID:31645178
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6928555/
Abstract

After cerebral ischemia, events like neural plasticity and tissue reorganization intervene in lesioned and non-lesioned areas of the brain. These processes are tightly related to functional improvement and successful rehabilitation in patients. Plastic remodeling in the brain is associated with limited spontaneous functional recovery in patients. Improvement depends on the initial deficit, size, nature and localization of the infarction, together with the sex and age of the patient, all of them affecting the favorable outcome of reorganization and repair of damaged areas. A better understanding of cerebral plasticity is pivotal to design effective therapeutic strategies. Experimental models and clinical studies have fueled the current understanding of the cellular and molecular processes responsible for plastic remodeling. In this review, we describe the known mechanisms, in patients and animal models, underlying cerebral reorganization and contributing to functional recovery after ischemic stroke. We also discuss the manipulations and therapies that can stimulate neural plasticity. We finally explore a new topic in the field of ischemic stroke pathophysiology, namely the brain-gut axis.

摘要

脑缺血后,神经可塑性和组织重组等事件会介入大脑受损和未受损区域。这些过程与患者的功能改善和成功康复密切相关。大脑中的塑性重塑与患者的有限自发性功能恢复有关。改善取决于初始缺陷、梗死的大小、性质和定位,以及患者的性别和年龄,所有这些都影响着受损区域的重组和修复的良好结果。更好地了解大脑的可塑性对于设计有效的治疗策略至关重要。实验模型和临床研究推动了对导致大脑可塑性的细胞和分子过程的理解。在这篇综述中,我们描述了已知的机制,在患者和动物模型中,大脑重组的基础和有助于缺血性中风后的功能恢复。我们还讨论了可以刺激神经可塑性的操作和治疗方法。最后,我们探索了缺血性中风病理生理学领域的一个新课题,即脑-肠轴。