• 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

中性粒细胞耗竭对局灶性缺血性中风后明胶酶表达、水肿形成及出血性转化的影响。

Effect of neutrophil depletion on gelatinase expression, edema formation and hemorrhagic transformation after focal ischemic stroke.

作者信息

Harris Alex K, Ergul Adviye, Kozak Anna, Machado Livia S, Johnson Maribeth H, Fagan Susan C

机构信息

Program in Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, Georgia, USA.

出版信息

BMC Neurosci. 2005 Aug 3;6:49. doi: 10.1186/1471-2202-6-49.

DOI:10.1186/1471-2202-6-49
PMID:16078993
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1190186/
Abstract

BACKGROUND

While gelatinase (MMP-2 and -9) activity is increased after focal ischemia/reperfusion injury in the brain, the relative contribution of neutrophils to the MMP activity and to the development of hemorrhagic transformation remains unknown.

RESULTS

Anti-PMN treatment caused successful depletion of neutrophils in treated animals. There was no difference in either infarct volume or hemorrhage between control and PMN depleted animals. While there were significant increases in gelatinase (MMP-2 and MMP-9) expression and activity and edema formation associated with ischemia, neutrophil depletion failed to cause any change.

CONCLUSION

The main finding of this study is that, in the absence of circulating neutrophils, MMP-2 and MMP-9 expression and activity are still up-regulated following focal cerebral ischemia. Additionally, neutrophil depletion had no influence on indicators of ischemic brain damage including edema, hemorrhage, and infarct size. These findings indicate that, at least acutely, neutrophils are not a significant contributor of gelatinase activity associated with acute neurovascular damage after stroke.

摘要

背景

虽然在脑局灶性缺血/再灌注损伤后明胶酶(基质金属蛋白酶-2和-9)活性增加,但中性粒细胞对基质金属蛋白酶活性及出血性转化发展的相对贡献仍不清楚。

结果

抗中性粒细胞治疗成功使治疗动物体内的中性粒细胞减少。对照动物和中性粒细胞减少的动物在梗死体积或出血方面均无差异。虽然与缺血相关的明胶酶(基质金属蛋白酶-2和基质金属蛋白酶-9)表达、活性及水肿形成有显著增加,但中性粒细胞减少并未引起任何变化。

结论

本研究的主要发现是,在没有循环中性粒细胞的情况下,局灶性脑缺血后基质金属蛋白酶-2和基质金属蛋白酶-9的表达及活性仍上调。此外,中性粒细胞减少对缺血性脑损伤指标(包括水肿、出血和梗死大小)没有影响。这些发现表明,至少在急性期,中性粒细胞不是与中风后急性神经血管损伤相关的明胶酶活性的重要贡献者。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4162/1190186/4da3228572b1/1471-2202-6-49-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4162/1190186/9c7216ed1a51/1471-2202-6-49-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4162/1190186/4ff5b0332405/1471-2202-6-49-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4162/1190186/1c81ba8ff036/1471-2202-6-49-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4162/1190186/00e8df1b64a4/1471-2202-6-49-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4162/1190186/4da3228572b1/1471-2202-6-49-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4162/1190186/9c7216ed1a51/1471-2202-6-49-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4162/1190186/4ff5b0332405/1471-2202-6-49-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4162/1190186/1c81ba8ff036/1471-2202-6-49-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4162/1190186/00e8df1b64a4/1471-2202-6-49-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4162/1190186/4da3228572b1/1471-2202-6-49-5.jpg

相似文献

1
Effect of neutrophil depletion on gelatinase expression, edema formation and hemorrhagic transformation after focal ischemic stroke.中性粒细胞耗竭对局灶性缺血性中风后明胶酶表达、水肿形成及出血性转化的影响。
BMC Neurosci. 2005 Aug 3;6:49. doi: 10.1186/1471-2202-6-49.
2
Microglial cell activation is a source of metalloproteinase generation during hemorrhagic transformation.小胶质细胞激活是出血性转化过程中金属蛋白酶生成的一个来源。
J Cereb Blood Flow Metab. 2012 May;32(5):919-32. doi: 10.1038/jcbfm.2012.11. Epub 2012 Feb 22.
3
Neutrophil infiltration increases matrix metalloproteinase-9 in the ischemic brain after occlusion/reperfusion of the middle cerebral artery in rats.大鼠大脑中动脉闭塞/再灌注后,中性粒细胞浸润增加缺血脑中的基质金属蛋白酶-9。
J Cereb Blood Flow Metab. 2003 Dec;23(12):1430-40. doi: 10.1097/01.WCB.0000090680.07515.C8.
4
Tumor necrosis factor-alpha neutralization reduced cerebral edema through inhibition of matrix metalloproteinase production after transient focal cerebral ischemia.肿瘤坏死因子-α 中和通过抑制短暂性局灶性脑缺血后基质金属蛋白酶的产生减轻脑水肿。
J Cereb Blood Flow Metab. 2005 Aug;25(8):959-67. doi: 10.1038/sj.jcbfm.9600086.
5
Reduced brain edema and matrix metalloproteinase (MMP) expression by pre-reperfusion infusion into ischemic territory in rat.通过在大鼠缺血区域进行再灌注前输注来减轻脑水肿和基质金属蛋白酶(MMP)表达。
Neurosci Lett. 2004 Nov 30;372(1-2):35-9. doi: 10.1016/j.neulet.2004.09.010.
6
Increased brain expression of matrix metalloproteinase-9 after ischemic and hemorrhagic human stroke.人类缺血性和出血性中风后基质金属蛋白酶-9在大脑中的表达增加。
Stroke. 2006 Jun;37(6):1399-406. doi: 10.1161/01.STR.0000223001.06264.af. Epub 2006 May 11.
7
Cerebral mast cells mediate blood-brain barrier disruption in acute experimental ischemic stroke through perivascular gelatinase activation.脑内肥大细胞通过血管周隙明胶酶激活介导急性实验性缺血性卒中的血脑屏障破坏。
Stroke. 2011 Dec;42(12):3600-5. doi: 10.1161/STROKEAHA.111.632224. Epub 2011 Oct 6.
8
Minocycline and hypothermia for reperfusion injury after focal cerebral ischemia in the rat: effects on BBB breakdown and MMP expression in the acute and subacute phase.米诺环素与低温对大鼠局灶性脑缺血后再灌注损伤的影响:对急性期和亚急性期血脑屏障破坏及基质金属蛋白酶表达的作用
Brain Res. 2008 Jan 10;1188:198-206. doi: 10.1016/j.brainres.2007.10.052. Epub 2007 Nov 26.
9
Metalloproteinase and stroke infarct size: role for anti-inflammatory treatment?金属蛋白酶与脑卒中梗死灶体积:抗炎治疗的作用?
Ann N Y Acad Sci. 2010 Oct;1207:123-33. doi: 10.1111/j.1749-6632.2010.05734.x.
10
Melatonin decreases matrix metalloproteinase-9 activation and expression and attenuates reperfusion-induced hemorrhage following transient focal cerebral ischemia in rats.褪黑素可降低大鼠短暂性局灶性脑缺血后基质金属蛋白酶-9的激活和表达,并减轻再灌注诱导的出血。
J Pineal Res. 2008 Nov;45(4):459-67. doi: 10.1111/j.1600-079X.2008.00617.x. Epub 2008 Jul 2.

引用本文的文献

1
Neutrophil Extracellular Traps Regulate Surgical Brain Injury by Activating the cGAS-STING Pathway.中性粒细胞胞外陷阱通过激活 cGAS-STING 通路调控外科性脑损伤。
Cell Mol Neurobiol. 2024 Apr 18;44(1):36. doi: 10.1007/s10571-024-01470-9.
2
Neutrophil dynamics and inflammaging in acute ischemic stroke: A transcriptomic review.急性缺血性卒中中的中性粒细胞动态变化与炎症衰老:一项转录组学综述
Front Aging Neurosci. 2022 Dec 22;14:1041333. doi: 10.3389/fnagi.2022.1041333. eCollection 2022.
3
Bone marrow-derived extracellular vesicles modulate the abundance of infiltrating immune cells in the brain and exert an antiviral effect against the Japanese encephalitis virus.

本文引用的文献

1
Targets for vascular protection after acute ischemic stroke.急性缺血性卒中后的血管保护靶点。
Stroke. 2004 Sep;35(9):2220-5. doi: 10.1161/01.STR.0000138023.60272.9e. Epub 2004 Jul 29.
2
Elastinolytic matrix metalloproteinases and their inhibitors as therapeutic targets in atherosclerotic plaque instability.
Cardiol Rev. 2004 May-Jun;12(3):141-50. doi: 10.1097/01.crd.0000105000.46909.81.
3
Matrix metalloproteinase-9 and myeloperoxidase expression: quantitative analysis by antigen immunohistochemistry in a model of transient focal cerebral ischemia.基质金属蛋白酶-9与髓过氧化物酶表达:短暂性局灶性脑缺血模型中抗原免疫组织化学定量分析
骨髓来源的细胞外囊泡可调节大脑中浸润免疫细胞的数量,并对日本脑炎病毒发挥抗病毒作用。
FASEB Bioadv. 2022 Oct 28;4(12):798-815. doi: 10.1096/fba.2022-00071. eCollection 2022 Dec.
4
Neutrophils delay repair process in Wallerian degeneration by releasing NETs outside the parenchyma.中性粒细胞通过向实质外释放 NETs 来延迟 Wallerian 变性的修复过程。
Life Sci Alliance. 2022 Aug 12;5(10). doi: 10.26508/lsa.202201399. Print 2022 Oct.
5
Inflammatory Responses After Ischemic Stroke.缺血性中风后的炎症反应。
Semin Immunopathol. 2022 Sep;44(5):625-648. doi: 10.1007/s00281-022-00943-7. Epub 2022 Jun 29.
6
Multiple Roles of Peripheral Immune System in Modulating Ischemia/Hypoxia-Induced Neuroinflammation.外周免疫系统在调节缺血/缺氧诱导的神经炎症中的多重作用
Front Mol Biosci. 2021 Nov 22;8:752465. doi: 10.3389/fmolb.2021.752465. eCollection 2021.
7
Pathophysiology of Blood-Brain Barrier Permeability Throughout the Different Stages of Ischemic Stroke and Its Implication on Hemorrhagic Transformation and Recovery.缺血性中风不同阶段血脑屏障通透性的病理生理学及其对出血性转化和恢复的影响
Front Neurol. 2020 Dec 9;11:594672. doi: 10.3389/fneur.2020.594672. eCollection 2020.
8
Alcohol exposure-induced neurovascular inflammatory priming impacts ischemic stroke and is linked with brain perivascular macrophages.酒精暴露诱导的神经血管炎症启动会影响缺血性中风,并与脑周细胞巨噬细胞有关。
JCI Insight. 2020 Feb 27;5(4):129226. doi: 10.1172/jci.insight.129226.
9
Peripheral myeloid cells contribute to brain injury in male neonatal mice.外周髓系细胞促进雄性新生期小鼠脑损伤。
J Neuroinflammation. 2018 Oct 30;15(1):301. doi: 10.1186/s12974-018-1344-9.
10
Pivotal role of innate myeloid cells in cerebral post-ischemic sterile inflammation.先天髓系细胞在脑缺血后无菌性炎症中的关键作用。
Semin Immunopathol. 2018 Nov;40(6):523-538. doi: 10.1007/s00281-018-0707-8. Epub 2018 Sep 11.
Stroke. 2004 May;35(5):1169-74. doi: 10.1161/01.STR.0000125861.55804.f2. Epub 2004 Apr 1.
4
Single slice method for quantification of hemorrhagic transformation using direct ELISA.使用直接酶联免疫吸附测定法对出血性转化进行定量的单层切片法
Neurol Res. 2004 Jan;26(1):93-8. doi: 10.1179/016164104773026606.
5
Neutrophil infiltration increases matrix metalloproteinase-9 in the ischemic brain after occlusion/reperfusion of the middle cerebral artery in rats.大鼠大脑中动脉闭塞/再灌注后,中性粒细胞浸润增加缺血脑中的基质金属蛋白酶-9。
J Cereb Blood Flow Metab. 2003 Dec;23(12):1430-40. doi: 10.1097/01.WCB.0000090680.07515.C8.
6
Hemorrhagic transformation is related to the duration of occlusion and treatment with tissue plasminogen activator in a nonembolic stroke model.在非栓塞性中风模型中,出血性转化与闭塞持续时间及组织型纤溶酶原激活剂治疗有关。
Neurol Res. 2003 Jun;25(4):377-82. doi: 10.1179/016164103101201526.
7
Stress upregulates arterial matrix metalloproteinase expression and activity via endothelin A receptor activation.
Am J Physiol Heart Circ Physiol. 2003 Nov;285(5):H2225-32. doi: 10.1152/ajpheart.00133.2003. Epub 2003 Jul 3.
8
Matrix metalloproteinases and tissue inhibitors of metalloproteinases: structure, function, and biochemistry.基质金属蛋白酶与金属蛋白酶组织抑制剂:结构、功能及生物化学
Circ Res. 2003 May 2;92(8):827-39. doi: 10.1161/01.RES.0000070112.80711.3D.
9
Amount of bleeding and hematoma size in the collagenase-induced intracerebral hemorrhage rat model.胶原酶诱导的脑出血大鼠模型中的出血量和血肿大小
Neurochem Res. 2003 May;28(5):779-85. doi: 10.1023/a:1022826220469.
10
Certain forms of matrix metalloproteinase-9 accumulate in the extracellular space after microdialysis probe implantation and middle cerebral artery occlusion/reperfusion.在微透析探针植入以及大脑中动脉闭塞/再灌注后,某些形式的基质金属蛋白酶-9会在细胞外间隙中积聚。
J Cereb Blood Flow Metab. 2002 Aug;22(8):918-25. doi: 10.1097/00004647-200208000-00003.