期刊文献+

大鼠脑出血后V_(1α)R和AQP4表达升高与脑水肿的形成相关 被引量:5

Increased expression of V_(1α) receptor and AQP4 are related to rat brain edema after intracerebral hemorrhage
下载PDF
导出
摘要 目的研究精氨酸加压素1α受体(V1αR)和水通道蛋白4(AQP4)在SD大鼠脑出血(ICH)脑组织中的表达变化及两者在脑水肿形成中的作用。方法将自体血注入大鼠尾状核建立脑出血模型,分别于术后6、12、24和48 h运用干湿重法、免疫荧光和Western blot检测脑含水量(BWC)、V1αR和AQP4蛋白的表达。结果脑出血后6 h,V1αR和AQP4的表达开始增加,至48 h达到高峰,分别为21.88±0.44和23.16±0.67,显著高于假手术组(14.32±0.55和13.90±0.40),与脑含水量呈正相关(P<0.05)。结论 V1αR介导的AQP4表达升高是脑出血后脑水肿形成的主要原因。 Objective To investigate the change of arginine-vasopressin Via receptor (V1α R)and aquaporin 4 (AQP4) expression, to explore the mechanism of brain edema caused by intracerebral hemorrhage(ICH). Methods Autologous blood were injected into the caudate nucleus to develope ICH model. The changes of brain water content (BWC)were measured by wet and dry weight methods. The expression of V1αR and AQP4 were detected by immu- nofluorescence and Western blot after 6, 12, 24 and 48 h. Results The expression of V1αR and AQP4 increased at 6h after ICH ,and significantly increased the peak at 48 h (21.88± 0. 44 and 23.16 ± 0. 67 )than the sham group ( 14. 52± 0. 55 and 15.90 ± 0. 40). V1α R and AQP4 expressions positively correlated with BWC ( P 〈 0. 05 ). Conclusions The increased expression of AQP4 mediated by V1αR plays an important role in the brain edema after ICH.
出处 《基础医学与临床》 CSCD 北大核心 2012年第9期1021-1025,共5页 Basic and Clinical Medicine
基金 国家自然科学基金(30470608)
关键词 精氨酸加压素 V1α受体 水通道蛋白4 脑水肿 arginine-vasopressin V1α receptor aquaporin 4 brain edema
  • 相关文献

参考文献12

  • 1Cheng CY, Chu JY, Chow BK. Vasopressin-independent mechanisms in controlling water homeostasis [ J ]. J Mol Endocrinol, 2009,43 : 81 - 92.
  • 2Taya K, Gulsen S, Okuno K, et al. Modulation of AQP4 ex- pression by the selective V1 α receptor antagonist, SR49059, decreases trauma-induced brain edema [ J ]. Ac- ta Neurochir Supp1,2009 ,102 :425 -429.
  • 3Liu XQ, Nakayama S, Amity MM, et al. Arginine-vasopressin V1 but not V2 receptor antagonism modulates infarct vol-ume, brain water content, and aquaporin-4 expression fol- lowing experimental stroke [ J ]. Neurocrit Care,2010,12 : 124 - 131.
  • 4Rynkowski MA, Kim GH, Komotar RJ,et al. A mouse model intracerebral hemorrhage using autologous blood infusion [ J]. Nature Protocol ,2008,3 : 122 - 127.
  • 5Tait M J, Saadoun S, Bell BA,et al. Increased brain edema in aqp4-null mice in an experimental model of subarachnoid hemorrhage [ J]. Neuroscience ,2010,167:60 - 67.
  • 6Haj-Yasein NN, Vindedal GF, Eilert-Olsen M, et al. Glial- conditional deletion of aquaporin-4 (Aqp4) reduces blood- brain water uptake and confers barrier function on perivas- cular astrocyte endfeet [ J ]. Proc Natl Acad Sci USA, 2011,108:1-6.
  • 7Papadopoulos MC, Verkman AS. Aquaporin-4 gene disrup- tion in mice reduces brain swelling and mortality in pneu- mococcal meningitis[ J]. J Biol Chem,2005,280 : 13906 - 13912.
  • 8Papadopoulos MC, Manley GT, Krishna S,et al. Aquaporin-4 facilitates reabsorption of excess fluid in vasogenic brain e- dema[ J]. FASEB J,2004,18 : 1291 - 1293.
  • 9Szmydynger CJ,Zink B J, Chodobski A. Multiple sites of vas-opressin synthesis in the injured brain [ J ]. J Cere Blood Flow Metab,2011,31:47 - 51.
  • 10Wang CJ, Creed C, Winklhofer FT, et al. Water prescription in autosomal dominant polycystic kidney disease:A Pilot Study [ J ]. CJASN,2011,6 : 192 - 197.

同被引文献47

引证文献5

二级引证文献15

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