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本文引用的文献

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Metabotropic glutamate receptor 5 deficiency inhibits neutrophil infiltration after traumatic brain injury in mice.代谢型谷氨酸受体 5 缺乏抑制小鼠创伤性脑损伤后的中性粒细胞浸润。
Sci Rep. 2017 Aug 30;7(1):9998. doi: 10.1038/s41598-017-10201-8.
2
Neutrophils Induce Astroglial Differentiation and Migration of Human Neural Stem Cells via C1q and C3a Synthesis.中性粒细胞通过C1q和C3a的合成诱导人神经干细胞的星形胶质细胞分化和迁移。
J Immunol. 2017 Aug 1;199(3):1069-1085. doi: 10.4049/jimmunol.1600064. Epub 2017 Jul 7.
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Blood-brain barrier dysfunction induced by silica NPs in vitro and in vivo: Involvement of oxidative stress and Rho-kinase/JNK signaling pathways.体外和体内二氧化硅纳米颗粒引起的血脑屏障功能障碍:氧化应激和 Rho-kinase/JNK 信号通路的参与。
Biomaterials. 2017 Mar;121:64-82. doi: 10.1016/j.biomaterials.2017.01.006. Epub 2017 Jan 4.
4
CXCL4 and CXCL4L1 Differentially Affect Monocyte Survival and Dendritic Cell Differentiation and Phagocytosis.CXCL4和CXCL4L1对单核细胞存活、树突状细胞分化及吞噬作用的影响存在差异。
PLoS One. 2016 Nov 9;11(11):e0166006. doi: 10.1371/journal.pone.0166006. eCollection 2016.
5
Activation of Adenosine 2A receptor inhibits neutrophil apoptosis in an autophagy-dependent manner in mice with systemic inflammatory response syndrome.腺苷 A2A 受体的激活以自噬依赖的方式抑制全身炎症反应综合征小鼠中性粒细胞的凋亡。
Sci Rep. 2016 Sep 20;6:33614. doi: 10.1038/srep33614.
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Pathophysiology and management of reperfusion injury and hyperperfusion syndrome after carotid endarterectomy and carotid artery stenting.颈动脉内膜切除术和颈动脉支架置入术后再灌注损伤及高灌注综合征的病理生理学与管理
Exp Transl Stroke Med. 2016 Sep 6;8(1):7. doi: 10.1186/s13231-016-0021-2. eCollection 2016.
7
Transfer of mitochondria from astrocytes to neurons after stroke.中风后星形胶质细胞的线粒体向神经元的转移。
Nature. 2016 Jul 28;535(7613):551-5. doi: 10.1038/nature18928.
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Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer's disease.在阿尔茨海默病的小鼠和线虫模型中,β淀粉样肽可抵御微生物感染。
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The blood-brain barrier.血脑屏障。
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Mechanism and Therapy of Brain Edema after Intracerebral Hemorrhage.脑出血后脑水肿的机制与治疗
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创伤性脑损伤 (TBI) 中的中性粒细胞:是敌是友?

Neutrophils in traumatic brain injury (TBI): friend or foe?

机构信息

Department of Biochemistry and Molecular Biology, Army Medical University, Chongqing, 400038, People's Republic of China.

Center for Pharmacogenetics, School of Pharmacy, University of Pittsburgh, Pittsburgh, Pennsylvania, 15261, USA.

出版信息

J Neuroinflammation. 2018 May 17;15(1):146. doi: 10.1186/s12974-018-1173-x.

DOI:10.1186/s12974-018-1173-x
PMID:29776443
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5960133/
Abstract

Our knowledge of the pathophysiology about traumatic brain injury (TBI) is still limited. Neutrophils, as the most abundant leukocytes in circulation and the first-line transmigrated immune cells at the sites of injury, are highly involved in the initiation, development, and recovery of TBI. Nonetheless, our understanding about neutrophils in TBI is obsolete, and mounting evidences from recent studies have challenged the conventional views. This review summarizes what is known about the relationships between neutrophils and pathophysiology of TBI. In addition, discussions are made on the complex roles as well as the controversial views of neutrophils in TBI.

摘要

我们对创伤性脑损伤 (TBI) 的病理生理学的了解仍然有限。中性粒细胞是循环中最丰富的白细胞,也是损伤部位第一时间迁移的免疫细胞,它们高度参与 TBI 的启动、发展和恢复。尽管如此,我们对 TBI 中性粒细胞的了解已经过时,最近的研究证据也对传统观点提出了挑战。本综述总结了目前已知的中性粒细胞与 TBI 病理生理学之间的关系。此外,还讨论了中性粒细胞在 TBI 中的复杂作用和有争议的观点。