期刊文献+

去铁胺干预对大鼠ICH后水通道蛋白4表达变化的影响 被引量:3

Effect of Deferoxamine on Aquaporin-4 Expression in a Rat Model of Intracerebral Haemorrhage
暂未订购
导出
摘要 目的观察水通道蛋白4(AQP4)在脑出血(ICH)模型组及去铁胺(DFO)干预组的表达变化及作用。方法采用自体血ICH模型,应用免疫组化及RT-PCR方法观察不同组别及时间段AQP4的表达。结果AQP4阳性细胞主要分布于脑内星形细胞足突与毛细血管接触区。AQP4蛋白表达在ICH模型组及DFO干预组均较假手术组明显增高且以第7天最高,DFO干预组第7及第14天AQP4蛋白表达较同期ICH模型组显著降低。AQP4 mRNA表达在所有ICH组及DFO干预第3及第7天组较假手术组显著增高且以第3天最高,ICH组第14与第7天AQP4 mRNA表达无显著差别。DFO干预各组与同期ICH模型组相比AQP4 mRNA表达显著降低,且DFO干预各组较前一时间点AQP4 mRNA表达呈显著下降趋势,DFO干预第14天组AQP4 mRNA表达与对照组无差别。AQP4蛋白表达与AQP4 mRNA表达呈正相关关系。结论AQP4在ICH后水肿的形成及消退中可能起重要作用,DFO可能对干预ICH后水肿形成有一定作用。 Objective To study the dynamic changes of AQP4 expression between Intracerebral Haemorrhage (ICH)models and Deferoxamine (DFO) intervention models. To explore the mechanism and role of AQP4 and DFO in edema formation after ICH. Methods ICH was established by infusing autologous blood into rat putamina; Immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) method were respectively used to evaluate AQP4 protein and mRNA expression in different group and distinct period of time. Results AQP4 positive cells mostly located in astrocyte in the perivascular glial feet processes in the brain. As compared with the sham operation groups, there appeared a significant increase of AQP4 protein expression in all ICH models and DFO intervention models; At 7 day, the AQP4 protein expression reached its maximum in ICH models and DFO intervention models; At 7 and 14 day, in DFO groups AQP4 protein expression decreased remarkably than ICH groups. There showed a significant enhanced expression of AQP4 mRNA in all ICH models and DFO intervention models at 3, 7 day compared with sham operation controls; At 3 day, AQP4 mRNA expression reached its maximum in ICH models and DFO intervention models; AQP4 mRNA expression decreased significantly in DFO models than ICH groups; There were descending trend in DFO models with the time extended; there were no differences between DFO models and controls at 14 day. There were positive correlations with AQP4 mRNA and AQP4 protein expression. Conclusions AQP4 may play a key role in edema formation and absorption after ICH, DFO was likely to be a new effective agent to intervene brain edema formation after ICH.
出处 《中国神经免疫学和神经病学杂志》 CAS 2006年第4期234-237,242,共5页 Chinese Journal of Neuroimmunology and Neurology
关键词 脑出血 脑水肿 水通道蛋白4(AQP4) 去铁胺(DFO) intracerebral hemorrhages brain edema aquaporin-4 deferoxamine
  • 相关文献

参考文献7

  • 1Tomas M,Venero JL,de Pablos RM,et al.In vivo expression of aquaporin-4 by reactive microglia[J].J Neurochem,2004,91(4):891-899.
  • 2张新江,殷小平,易黎,张苏明,方思羽,卢广.大鼠缓慢注射自体血脑出血模型[J].中风与神经疾病杂志,2002,19(5):299-301. 被引量:30
  • 3Nakamura T,Keep RF,Hua Y,et al.Deferoxamineinduced attenuation of brain edema and neurological deficits in a rat model of intracerebral hemorrhage[J].J Neurosurg,2004,100(4):672-678.
  • 4Berderson JB,Pits LH,Tsuji M,et al.Rat middle cerebral artery occlusion:evaluation of the model and development of a neurologic examination[J].Stroke,1986,17:472-476.
  • 5李燕华,孙善全.实验性脑出血后水通道蛋白-4的表达变化[J].中华神经科杂志,2004,37(2):144-148. 被引量:55
  • 6Lo AC,Chen AY,Hung VK,et al.Endothelin-1overexpression leads to further water accumulation and brain edema after middle cerebral artery occlusion via aquaporin 4 expression in astrocytic end-feet[J].J Cereb Blood Flow Metab,2005,25(8):998-1011.
  • 7Griesdale DEG,Honey CR.Aquaporins and brain edema[J].Surg Neurol,2004,61(5):418-421.

二级参考文献21

  • 1汤继宏,刘春风,张志琳,包仕尧.大鼠脑尾状核出血的模型[J].临床神经病学杂志,1996,9(3):134-135. 被引量:9
  • 2Manley GT, Fujimura M, Ma T, et al. Aquaporin-4 deletion in mice reduces brain edema after acute water toxication and ischemic stroke. Nat Med, 2000, 6: 159-163.
  • 3Rosenberg GA, Mun-Bryce S, Wesley M, et al. Collagenase induced intracerebral hemorrhage in rats. Stroke, 1990, 21: 802-807.
  • 4Bederson JB, Pitts LH, Nishimura MC, et al. Rat middle cerebral artery occlusion: evaluation of the model and development of a neurologic examination. Stroke, 1986, 17: 472-477.
  • 5Yang GY, Betz AL, Chenevert TL, et al. Experimental intracerebral hemorrhage:relationship between brain edema,blood flow,and blood-brain barrier permeability in rats. J Neurosurg, 1994, 81: 93-102.
  • 6Xue M, Del B. Acute tissue damage after injection of thrombin and plasmin into rat striatum. Stroke, 2001, 32: 2164-2168.
  • 7Wagner KR, Xi G, Hua Y, et al. Early metabolic alterations in edematous perihematomal brain regions following experimental intracerebral hemorrhage. J Neurosurg, 1998, 88: 1058-1065.
  • 8King LS, Agre P. Pathophysiology of the aquaporin water channels. Annu Rev Physiol, 1996, 58: 619-622.
  • 9Verkman AS. Physiological importance of aquaporin water channels. Ann Med, 2002, 34: 192-200.
  • 10Taniguchi M, Yamashita T, Kumura E, et al. Induction of aquaporin-4 water channel mRNA after focal cerebral ischemia in rat. Brain Res Mol Brain Res, 2000, 78: 131-137.

共引文献81

同被引文献41

  • 1徐如祥.创伤性脑水肿研究进展[J].中国现代神经疾病杂志,2004,4(3):141-145. 被引量:19
  • 2金露,李敬波,闻树群,黄鉴政.铁螯合剂对大鼠脑出血脑水肿的治疗作用[J].实用医学杂志,2005,21(21):2409-2411. 被引量:2
  • 3Mehdiratta M, Kumar S, Hackney D, et al, Association between serum ferritin level and perihematoma edema volume in patients with spontaneous intracerebral hemorrhage. Stroke, 2008, 39:1165-1170.
  • 4Heo JH, Han SW, Lee SK. Free radicals as triggers of brain edema formation after stroke. Free Radic Biol Med, 2005, 39: 51-70.
  • 5Huang FP, Xi G, Keep RF, et al. Brain edema after experimental intracerebral hemorrhage: role of hemoglobin degradation products. J Neurosurg, 2002, 96: 287-293.
  • 6Nakamura T, Xi G, Park JW, et al. Holo-transferrin and thrombin can interact to cause train damage. Stroke, 2005, 36: 348-352.
  • 7Whittaker JW. The irony of manganese superoxide dismutase. Biochem Soc Trans, 2003, 31: 1318-1321.
  • 8Nakamura T, Keep RF, Hua Y, et al. Oxidative DNA injury after experimental intracerebral.hemorrhage. Brain Res, 2005, 1039: 30- 36.
  • 9Gamez A, Carbonell T, Rama R. Does nitric oxide contribute to iron-dependent brain injury after experimental cerebral isehaemia? J Physiol Biochem, 2003, 59: 249-254.
  • 10Akool el-S, Kleinert H, Hamada FM, et al. Nitric oxide increases the decay of matrix metalloproteinase 9 mRNA by inhibiting the expression of mRNA-stabilizing factor HuR. Mol Cell Biol, 2003, 23:4901-4916.

引证文献3

二级引证文献8

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