大鼠弥漫性脑损伤后水通道蛋白4的表达
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摘要
目的观察大鼠弥漫性脑损伤后水通道蛋白4(aquaporin 4,AQP4)的表达,探讨其在脑水肿发生中的作用。方法参照Marmarou的打击负荷伤模型,建立大鼠弥漫性脑损伤动物模型。用干湿重法测定脑组织含水量,用伊文思蓝(Evans blue,EB)检测血脑屏障通透性的变化,运用免疫组织化学方法观察AQP4的表达。结果打击后3 h脑组织含水量增加,24 h达到高峰。脑组织EB含量伤后明显增加,12 h达到高峰。AQP4于打击后3 h表达明显增强,24 h达到高峰,AQP4阳性表达的胶质细胞数量明显增多。结论大鼠弥漫性脑损伤后血脑屏障通透性的增加及AQP4表达的增强促进脑水肿的发生,AQP4在胶质细胞的表达变化可用于辅助诊断弥漫性脑损伤。
Objective To observe the expression of aquaporin 4(AQP4) in diffuse brain injury(DBI) of rats and to explore the corresponding effect of AQP4 for brain edema. Methods The rat model of DBI was established using Marmarou's impact-compression trauma model. Brain water content was measured by dry-wet weight method. Blood-brain barrier permeability was evaluated by Evans blue(EB) staining.Immunohistochemical method was used to observe the expression of AQP4. Results Brain water content increased after 3 h and peaked at 24 h after DBI. Brain EB content significantly increased and peaked at12 h after DBI. The expression of AQP4 significantly increased after 3 h and peaked at 24 h after DBI,and the number of AQP4 positive astrocytes increased. Conclusion The increment of the permeability of blood-brain barrier and the expression of AQP4 may contribute to the development of brain edema in rat DBI. The change of AQP4 expression in astrocytes may also contribute to determine DBI.
Objective To observe the expression of aquaporin 4(AQP4) in diffuse brain injury(DBI) of rats and to explore the corresponding effect of AQP4 for brain edema. Methods The rat model of DBI was established using Marmarou's impact-compression trauma model. Brain water content was measured by dry-wet weight method. Blood-brain barrier permeability was evaluated by Evans blue(EB) staining.Immunohistochemical method was used to observe the expression of AQP4. Results Brain water content increased after 3 h and peaked at 24 h after DBI. Brain EB content significantly increased and peaked at12 h after DBI. The expression of AQP4 significantly increased after 3 h and peaked at 24 h after DBI,and the number of AQP4 positive astrocytes increased. Conclusion The increment of the permeability of blood-brain barrier and the expression of AQP4 may contribute to the development of brain edema in rat DBI. The change of AQP4 expression in astrocytes may also contribute to determine DBI.
引文
[1]Graham DI,Mc Intosh TK,Maxwell WL,et al.Recent advances in neurotrauma[J].J Neuropathol Exp Neurol,2000,59(8):641-651.
[2]Papadopoulos MC,Verkman AS.Aquaporin-4 and brain edema[J].Pediatr Nephrol,2007,22(6):778-784.
[3]Foda MA,Marmarou A.A new model of diffuse brain injury in rats.PartⅡ:Morphological characterization[J].J Neurosurg,1994,80(2):301-313.
[4]Uyama O,Okamura N,Yanase M,et al.Quantitative evaluation of vascular permeability in the gerbil brain after transient ischemia using Evans blue fluorescence[J].J Cereb Blood Flow Metab,1988,8(2):282-284.
[5]申洪,陆药丹.免疫组织化学染色的定量方法研究[J].生物医学工程学杂志,1993,10(3):281-284.
[6]惠国桢,吴思荣.弥漫性脑损伤的研究与治疗[J].中华创伤杂志,2004,20(6):323-325.
[7]石向群,杨金升,张志琳,等.水通道蛋白-4在正常大鼠脑内的分布研究[J].中华神经医学杂志,2004,3(4):257-259.
[8]张琳,袁芳.大鼠脑外伤诱导水通道蛋白4表达增强加重脑水肿[J].首都医科大学学报,2008,29(6):732-736.
[9]Wang Z,Meng CJ,Shen XM,et al.Potential contribution of hypoxia-inducible factor-1α,aquaporin-4,and matrix metalloproteinase-9 to blood-brain barrier disruption and brain edema after experimental subarachnoid hemorrhage[J].J Mol Neurosci,2012,48(1):273-280.
[10]Taya K,Marmarou CR,Okuno K,et al.Effect of secondary insults upon aquaporin-4 water channels following experimental cortical contusion in rats[J].J Neurotrauma,2010,27(1):229-239.
[2]Papadopoulos MC,Verkman AS.Aquaporin-4 and brain edema[J].Pediatr Nephrol,2007,22(6):778-784.
[3]Foda MA,Marmarou A.A new model of diffuse brain injury in rats.PartⅡ:Morphological characterization[J].J Neurosurg,1994,80(2):301-313.
[4]Uyama O,Okamura N,Yanase M,et al.Quantitative evaluation of vascular permeability in the gerbil brain after transient ischemia using Evans blue fluorescence[J].J Cereb Blood Flow Metab,1988,8(2):282-284.
[5]申洪,陆药丹.免疫组织化学染色的定量方法研究[J].生物医学工程学杂志,1993,10(3):281-284.
[6]惠国桢,吴思荣.弥漫性脑损伤的研究与治疗[J].中华创伤杂志,2004,20(6):323-325.
[7]石向群,杨金升,张志琳,等.水通道蛋白-4在正常大鼠脑内的分布研究[J].中华神经医学杂志,2004,3(4):257-259.
[8]张琳,袁芳.大鼠脑外伤诱导水通道蛋白4表达增强加重脑水肿[J].首都医科大学学报,2008,29(6):732-736.
[9]Wang Z,Meng CJ,Shen XM,et al.Potential contribution of hypoxia-inducible factor-1α,aquaporin-4,and matrix metalloproteinase-9 to blood-brain barrier disruption and brain edema after experimental subarachnoid hemorrhage[J].J Mol Neurosci,2012,48(1):273-280.
[10]Taya K,Marmarou CR,Okuno K,et al.Effect of secondary insults upon aquaporin-4 water channels following experimental cortical contusion in rats[J].J Neurotrauma,2010,27(1):229-239.