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脑卒中后炎性因素的变化 被引量:1

Changes of inflammatory factors after stroke
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摘要 目的观察炎性因素在卒中后脑组织中的存在时间及分布特点。方法卒中尸检脑9例,用免疫组化方法标记炎细胞及炎性因子。结果小胶质细胞激活出现于梗死后10h,2d后逐渐分布于周边区。肿瘤坏死因子α主要由星形细胞表达。星形细胞在中心区消失,周边区增生。吞噬细胞于缺血1d始分布于梗死中心区。白细胞共同抗原仅在出血病灶周边表达。结论人脑梗死后10h起即有炎性因素变化,2d之内主要分布在中心区,2d后主要分布在周边区。直接破入或穿过内皮细胞的连接进入脑组织的血源性白细胞的共同抗原的表达有所不同。 Objective To observe the changes of mieroglia, astrecyte, macrophage, TNFα and TGFβ and discuss the role of inflammation caused by cerebral infarction. Methods Nine autopsy brains were included (7 cerebral infarction, 2 cerebral hemorrhage). The SP method of immunohistocbemistry was used for CD68, GFAP, TNF and TGF. Results The mieroglia activation began from 10 hours after infarction, move from iscbemia core towards the border area after 2 days, and lots expressed on the surrounding area after 2 weeks. Astrocytes disappeared in the isebemia core and hyperplasia on the surrounding area. The hyperplasie glia cells have different shape at different isebemia time. TNFα are mainly expressed by astrocyte. The hippocampus also express TNFα2 ease in the same side and 4 ease in the opposite. Macrophage distribute in the ischemia core after 24 hours. The leukocyte common antigen expressions are positive in the surrounding area of hemorrhage brain and negative in the iscbemia brain. TGFβ expression is mainly around the iscbemia area. Condusion The human have had the inflammation changing at 10 h after cerebral infarction, mainly distributed in the ischemia core within 2 days, and moved towards the surrounding area after 2 days. The LCA expressions of the inflammation cells might be different between the different invading methods of rupturing directly or transferring through the endothelia iunction.
出处 《中华神经科杂志》 CAS CSCD 北大核心 2005年第12期755-758,共4页 Chinese Journal of Neurology
基金 国家自然科学基金资助项目(30470618)
关键词 脑血管意外 小神经胶质细胞 细胞因子类 Cerebrovascular accident Microglia Cytokines
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参考文献13

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共引文献38

同被引文献6

  • 1张星虎.炎性反应与动脉粥样硬化[J].中国卒中杂志,2008,3(6):408-412. 被引量:4
  • 2Nakase T, Yazamaki T, Qura N, et al. The impact of inflammation on the pathogenesis and prognosis of ischemic stroke. J Ncurol Sci, 2008, 271 (2): 104-109.
  • 3Terao S, Yilmaz G, Stokes KY, et a l. Blood cellderived RANTES mediates cerebral mierovascular dysfunction, inflammation and tissue injury after fooal isehemia reperfusion. Stoke, 2008, 39(2) : 2560-2570.
  • 4Bone RC, Balk RA, Cera FB, et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest, 1992, 101(6) : 1644-1655.
  • 5Dhar R, Michael N. The Burden of the Systemic Inflammatory Response Predicts Vasospasm and Outcome after Subaraehnoid Hemorrhage. Neurocritical Care, 2008, 8 ( 3 ) : 404-412.
  • 6刘其春,肖慧,唐春柳,谷文萍.脑缺血后炎症反应及其治疗前景[J].国际神经病学神经外科学杂志,2009,36(1):59-62. 被引量:10

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