[1]王世召 张立民 张云鹤 综述 付爱军 审校.血脑屏障与免疫炎症反应[J].中国临床神经外科杂志,2015,(07):439-442.[doi:10.13798/j.issn.1009-153X.2015.07.021]
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血脑屏障与免疫炎症反应()
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《中国临床神经外科杂志》[ISSN:1009-153X/CN:42-1603/TN]

卷:
期数:
2015年07期
页码:
439-442
栏目:
论著
出版日期:
2015-07-30

文章信息/Info

文章编号:
1009-153X(2015)05-0439-04
作者:
王世召 张立民 张云鹤 综述 付爱军 审校
063000 河北唐山,华北理工大学附属医院神经外科
通讯作者:付爱军,E-mail:wsz1987315@163.com
关键词:
血脑屏障炎症反应关系
分类号:
R 741.02; R 346.5
DOI:
10.13798/j.issn.1009-153X.2015.07.021
文献标志码:
B

参考文献/References:

[1] Obermeier B, Daneman R, Ransohoff RM. Development, maintenance and disruption of the blood-brain barrier [J]. Nat Med, 2013, 19(12): 1584-1596.
[2] Yang Y, Thompson JF, Taheri S, et al. Early inhibition of MMP activity in ischemic rat brain promotes expression of tight junction proteins and angiogenesis during recovery [J]. J Cereb Blood Flow Metab, 2013, 33(7): 1104-1114.
[3] Bauer AT, Burgers HF, Rabie T, et al. Matrix metallopro- teinase-9 mediates hypoxia-induced vascular leakage in the brain via tight junction rearrangement [J]. J Cereb Blood Flow Metab, 2010, 30: 837-848.
[4] Su JJ, O soegawa M, Mat suoka T, et al. Upregulation of vascular growth factors in multiple sclerosis: correlation with MRI findings [J]. J Neurol Sci, 2006, 243: 21-30.
[5] Argaw AT, Gurfe in BT, Zhang Y, et al. VEGF-mediated disruption of endothelial CLN-5 promotes blood-brain barrier breakdown [J]. Proc Natl Acad Sci USA, 2009, 106: 1977-1982.
[6] Fischer S, Wiesnet M, Marti HH, et al. Simultaneous activa- tion of several second messengers in hypoxia-induced hy- perpermeability of brain derived endothelial cells [J]. J Cell Physiol, 2004, 198(3): 359-369.
[7] Maier CM, Hsieh L, Crandall T, et al. Evaluating therapeu- tic targets for reperfusion-related brain hemorrhage [J]. Ann Neurol, 2006, 59: 929-938.
[8] Lee HS, Namkoong K, Kim DH, et al. Hydrogen peroxide- induced alterations of tight junction proteins in bovine brain microvascular endothelial cells [J]. Microvasc Res, 2004, 68: 231-238.
[9] Schreibelt G, Kooij G, Reijerkerk A, et al. Reactive oxygen species alter brain endothelial tight junction dynamics via RhoA, PI3 kinase, and PKB signaling [J]. FASEB J, 2007, 21: 3666-3676.
[10] Gobel K, Pankratz S, Schneider-Hohendorf T, et al. Bloc- kade of the kinin receptor B1 protects from autoimmune CNS disease by reducing leukocyte trafficking [J]. J Autoi- mmun, 2011, 36: 106-114.
[11] Mankertz J, Tavalali S, Schmitz H, et al. Expression from the human occludin promoter is affected by tumor necrosis factor alpha and interferon gamma [J]. J Cell Sci, 2000, 113 (11): 2085-2090.
[12] Sozen T, Tsuchiyama R, Hasegawa Y, et al. Role of inter- leukin-1beta in early brain injury after subarachnoid hemorrhage in mice [J]. Stroke, 2009, 40: 2519-2525.
[13] McColl BW, Rothwell NJ, Allan SM. Systemic inflammation alters the kinetics of cerebrovascular tight junction disrup- tion after experimental stroke in mice [J]. J Neurosci, 2008, 28: 9451-9462.
[14] Bart holomaus I, Kawa kami N, Odoardi F, et al. Effector T cell interactions with meningeal vascular structures in nascent autoimmune CNS lesions [J]. Nature, 2009, 462: 94-98.
[15] Kivisakk P, Imitola J, Rasmussen S, et al. Localizing central nervous system immune surveillance: meningeal antigen- presenting cells activate T cells during experimental auto- immune encephalomyelitis [J]. Ann Neurol, 2009, 65: 457- 469.
[16] Doring A, Wild M, Vestweber D, et al. E-and P-selectin are not required for the development of experimental auto- immune encephalomyelitis in C57BL/6 and SJL mice [J]. J Immunol, 2007, 179: 8470-8479.
[17] Cramer SP, Simonsen H, Frederiksen JL, et al. Abnormal blood-brain barrier permeability in normal appearing white matter in multiple sclerosis investigated by MRI [J]. Neuro- image Clin, 2013, 4: 182-189.
[18] Erickson MA, Banks WA. Blood-brain barrier dysfunction as a cause and consequence of Alzheimer's disease [J]. J Cereb Blood Flow Metab, 2013, 33(10): 1500-1513.

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更新日期/Last Update: 2015-07-30