期刊文献+

局灶性脑缺血再灌注后炎症反应及黏附分子、环氧合酶-2的表达 被引量:1

Inflammatory reaction and expression of adhesion molecules and cyclooxygenase-2 after reperfusion in focal cerebral ischemia rats
原文传递
导出
摘要 目的探讨环氧合酶2(COX2)和黏附分子在再灌注后炎症损伤中的作用。方法线栓法制作大鼠大脑中动脉缺血模型(MCAO)。用免疫印迹及免疫组化方法观察再灌注后不同时间脑组织细胞间黏附分子1(ICAM1)、E选择素及COX2的表达。白细胞髓过氧化物酶(MPO)检测试剂盒检测MPO活性。结果假手术组及再灌注4、22、46h组,缺血脑皮质及纹状体中COX2含量相对灰度值分别为0.7642±0.0763、1.5382±0.1047、1.6491±0.3265、1.8020±0.3719及0.7104±0.0891、2.2061±0.2143、1.7897±0.3537、1.8018±0.5703;ICAM1相对灰度值分别为0.6845±0.0531、0.9115±0.0422、0.9426±0.0407、1.0756±0.0467及0.6583±0.0361、0.9439±0.0746、0.9975±0.1532、0.8808±0.0497。再灌注各组MPO活性、COX2、ICAM1和E选择素表达均较假手术组高。免疫组化显示,缺血再灌注后,缺血边缘区出现大量E选择素和ICAM1免疫染色阳性的微血管,在皮质的COX2阳性细胞主要为神经元,纹状体出现了免疫阳性的胶质细胞和血管内皮细胞。再灌注后不同时间皮质COX2与ICAM1表达量呈正相关(n=6,r=0.973,P<0.05);纹状体COX2与E选择素表达量呈正相关(n=6,r=0.958,P<0.05)。结论炎症反应参与了缺血周边区的再灌注后继发性损伤,COX2和内皮黏附分子的表达都在再灌注后炎症反应中发挥重要的作用。 Objective To clarify the possible role of cyclooxygenase-2 (COX-2), intercellular adhesion moleeule-1 (ICAM-1) and E-seleetin in the inflammatory injury indueed by eerebral isehemia and reperfusion. Methods The focal cerebral ischemia and reperfusion model was induced by a suture occlusion of the right middle cerebral artery. The rats were randomly assigned to four groups: sham operated group; 4 h,22 h and 46 h reperfusion groups. The expression of ICAM-1, E-selectin and COX-2 were detected by immuno-Western blot and immunohistochemical method. Myeloperoxidase (MPO) activity was detected by a commercial MPO kit. Results In the fight cortex and striatum of the sham operated group and the 4 h,22 h and 46 h reperfusion groups, the relative values of COX-2 were 0. 7642 ± 0. 0763, 1. 5382 ± 0. 1047, 1. 6491 ± 0. 3265, 1. 8020 ± 0. 3719 and 0. 7104 ± 0. 0891, 2. 2061 ± 0. 2143, 1. 7897 ± 0. 3537, 1. 8018 ± 0. 5703 respectively; the relative values of ICAM-1 were 0. 6845 ± 0. 0531, 0. 9115 ± 0. 0422, 0. 9426 ± 0.0407, 1.0756 ±0.0467 and 0.6583 ±0.0361, 0.9439 ±0.0746, 0.9975 ±0. 1532, 0. 8808±0.0497 respectively. Significant increase of MPO activity and expression levels of COX-2, ICAM-1 and E-selectin were shown from 4 h to 46 h in the striatum and cortex of rats following reperfusion, hnmunohistochemical staining showed that the number of ICAM-1 and E-selectin positive vessels was increased in the border of ischemia. The positive cells of COX-2 were almost neurons in the cortex, but in the striatum, the cells were neurons, glias and vessel endothelium. Positive eorrelation between COX-2 and ICAM-1 expression in the cortex ( n = 6, r = 0. 973,P 〈 0.05 ) was noted, and COX-2 and E-selectin in the striatum as well ( n = 6, r = 0. 958 ,P 〈 0.05). Conclusions Inflammatory reaction might be involved in secondary brain injury after cerebral ischemia and reperfusion. The adhesion molecules and COX-2 should be the same important roles in this process.
出处 《中华神经科杂志》 CAS CSCD 北大核心 2005年第10期632-635,共4页 Chinese Journal of Neurology
关键词 脑缺血 再灌注 胞间黏附分子1 前列腺素内过氧化物合酶 Brain ischemia Reperfusion Intercellular adhesion molecule-l Prostaglandin-endoperoxide synthase
  • 相关文献

参考文献8

  • 1Longa EZ, Weinstein PR, Carlson S. Reversible middle cerebral artery occlusion without craniectomy in rats. Stroke, 1989,20:84-91. 被引量:1
  • 2Zhang RL, Chopp M, Chen H, et al. Temporal profile of ischemic tissue damage, neutrophile response, and vascular plugging following permanent and transient (2H) middle cerebral artery occlusion in the rat. J Neurol Sci,1994,125:3-10. 被引量:1
  • 3Jean WC, Spellman SR, Nussbaum ES, et al. Reperfusion injury after focal cerebral ischemia: the role of inflammation and the therapeutic horizon Neurosurgery,1998,43:1382-1397. 被引量:1
  • 4Zhang L, Zhang ZG, Zhang RL,et al. Effects of a selective CDllb/CD18 antagonist and recombinant human tissue plasminogen activator treatment alone and in combination in a rat embolic model of stroke.Stroke ,2003,34 : 1790-1795. 被引量:1
  • 5Stanimirovic D, Satoh K. Inflammatory mediators of cerebral endothelium: a role in ischemic brain inflammation. Brain Pathol,2000,10: 113-126. 被引量:1
  • 6Wang Q, Doerschuk CM. The signaling pathways induced by neutrophil-endothelial cell adhesion. Antioxid Redox Signal, 2002,4:39-47. 被引量:1
  • 7Zhang W, Smith C, Monette R, et al. Indomethacin and cyclosporin a inhibit in vitro ischemia-induced expression of ICAM-1 and chemokines in human endothelial cell. Acta Neurochir Suppl, 2000,76: 47-53. 被引量:1
  • 8Planas AM, Soriano MA, Justicia C, et al. Induction of cyclooxygenase-2 in the rat brain after a mild episode of focal ischemia without tissue inflammation or neural cell damage. Neurosci Lett, 1999,275 : 141-144. 被引量:1

同被引文献12

  • 1杨杰,侯晓华.环氧合酶与胃粘膜防御[J].国际消化病杂志,2006,26(2):101-104. 被引量:6
  • 2Guo Y, Bao W, Wu WJ, et al. Evidence for an essential role of cyclooxygenase-2 as a mediator of the late phase of ischemic preconditioning in mice [ J ]. Basic Res Cardiol, 2000, 95 (6) : 479484. 被引量:1
  • 3Ma W, Eisenach JC. Cyclooxygenase 2 in infiltrating inflammatory cells in injured nerve is universally up- regulated following various types of peripheral nerve injury [J]. Neuroscience, 2003, 121 (3): 691-704. 被引量:1
  • 4Yokoyama T, Aramaki O, Takayama T, et al. Selective cyclooxygenase 2 inhibitor induces indefinite survival of fully allogeneic cardiac grafts and generates CD4 + regulatory cells[J]. J Thorac Cardiovasc Surg, 2005, 130 (4) : 1167-1174. 被引量:1
  • 5Dallal O, Ravindranath TM, Choudhry MA, et al. T-cell proliferative responses following sepsis in neonatal rats [ J ]. Biol Neonate, 2003, 83 (3) : 201-207. 被引量:1
  • 6Knoferl MW, Diodato MD, Schwacha MG, et al. Cyclooxy- genase-2-mediated regulation of Kupffer cell interleukin-6 production following trauma-hemorrhage and subsequent sepsis[J]. Shock, 2001, 16 (6) : 479-483. 被引量:1
  • 7Osterberg J, Ljungdahl M, Haglund U. Influence of cyclo-oxygenase inhibitors on gut immune cell distribution and apoptosis rate in experimental sepsis [ J ]. Shock, 2006, 25 (2) : 147-154. 被引量:1
  • 8Bone RC. Immunologic dissonance: a continuing evolution in our understanding of the systemic inflammatory response syndrome (SIRS) and the multiple organ dysfunction syndrome (MODS) [J]. Ann Intern Med, 1996, 125 (8) : 680-687. 被引量:1
  • 9Goldie AS, Fearon KC, Ross JA, et al. Natural cytokine antagonists and endogenous antiendotoxin core antibodies in sepsis syndrome. The Sepsis Intervention Group [ J ]. JAMA, 1995, 274 (2): 172-177. 被引量:1
  • 10Doughty LA, Kaplan SS, Carcillo JA. Inflammatory cytokine and nitric oxide responses in pediatric sepsis and organ failure[J]. Crit Care Med, 1996, 24 (7) : 1137-1143. 被引量:1

引证文献1

二级引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部