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大鼠创伤性脑损伤中内皮性脂酶表达变化

Expression of endothelial lipase in rat traumatic brain injuried
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摘要 目的探讨内皮性脂酶(EL)在创伤性脑损伤(TBI)后的表达变化及定位情况。方法应用健康成年SD大鼠40只,成功制备TBI模型31只。通过Western blotting检测脑损伤后EL表达的时相变化,免疫荧光化学方法检测EL在脑组织中的细胞定位。结果 Western blotting显示,大鼠脑损伤后,EL表达逐步增高,伤后3d升至最高点,之后逐渐下降,于损伤后2周时降至最低水平;免疫荧光双标记结果显示EL与神经元的标记物NeuN共定位。与凋亡相关的蛋白Caspase-3和Bcl-2在TBI后表达发生变化,并且细胞凋亡趋势与EL表达变化趋势基本一致。结论大鼠TBI后,EL表达增加,推测EL可能参与脑损伤后神经再生及神经元凋亡过程。 Objeetive To investigate the expression of Endothelial Lipase (EL) in rat brains after being injuried. Methods Forty healthy adult SD rats were used, thirty one rats were successfully prepared as traumatic brain injury (TBI) model. The expression of EL was tested by Western blotting at various time points after injury. Double immunofluorescent staining was used to observe the cell distribution of EL as well as changes in expression levels after injury. Results Western blotting data showed that EL proteins in lesion site increased gradually and reached a peak on the 3rd day post injury, and it decreased to the lowest level until 2 weeks after the injury. EL was localized in neurons as shown by co-localization with neuronal nuclei (NeuN). Intensity of immunofluorescence was weak in intact brain but greatly enhanced on the 3rd day after the injury. In addition, temporal expression pattern of Caspase-3, a key protein involved in apoptosis, was similar to that of EL, and expression of Bcl-2, which is involved in anti-apoptosis was also temporally regulated. Conclusion The brain injury results in up-regulation of EL expression in traumatic brain sites suggesting that it may participate in brain injury-induced apoptosis as well as neuronal regeneration processes.
出处 《解剖学报》 CAS CSCD 北大核心 2011年第3期314-317,共4页 Acta Anatomica Sinica
基金 国家自然科学基金资助项目(30772242)
关键词 创伤性脑损伤 脂质代谢:内皮性脂酶 免疫印迹法 免疫荧光 大鼠 Traumatic brain injury Lipid metabolism Endothelial lipase Western blotting Immunofluorescence Rat
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参考文献12

  • 1Marshall LF.Epidemiology and cost of central nervous system injury[J].Clin Neurosurg,2000,46(1):105-112.
  • 2McCarty JH.Cell adhesion and signaling networks in brain neurovascular units[J].Curr Opin Hematol,2009,16(3):209-214.
  • 3Vance JE.Lipid imbalance in the neurological disorder,Niemann-Pick C disease[J].FEBS Letts,2006,580(23):5518-5524.
  • 4胥学伟,李小鹰.甘油三酯脂酶家族中的新成员——内皮源性脂酶[J].中国分子心脏病学杂志,2003,3(6):359-362. 被引量:1
  • 5Paradis E,Clavel S,Julien P,et al.Lipoprotein lipase and endothelial lipase expression in mouse brain:regional distribution and selective induction following kainic acid-induced lesion and focal cerebral ischemia[J].Neurobiol Dis,2004,15(2):312-325.
  • 6Logan A,Frautschy SA,Gonzalez AM,et al.A time course for the focal elevation of synthesis of basic fibroblast growth factor and one of its high-affinity receptors (flg) following a localized cortical brain injury[J].J Neurosci,1992,12(10):3828-3837.
  • 7Mattson MP,Cutler RG,Jo DG.Alzheimer peptides perturb lipid-regulating enzymes[J].Nat Cell Biol,2005,7(11):1045-1047.
  • 8Adibhatla RM,Hatcher JF,Dempsey RJ.Lipids and lipidomics in brain injury and diseases[J].AAPS J,2006,8(2):314-321.
  • 9Adibhatla RM,Hatcher JF,Dempsey RJ.Role of lipids in brain injury and diseases[J].Future Lipidol,2007,2(4):403-422.
  • 10Eldadah BA,Faden AI.Caspase pathways,neuronal apoptosis,and CNS injury[J].J Neurotrauma,2000,17(10):811-829.

二级参考文献10

  • 1Clark RSB,Kochanek PM,Adelson PD,et al.Increases in Bcl-2 protein in cerebrospinal fluid and evidence for programmed cell death in infants and chidren following severe traumatic brain injury[].The Journal of Pediatrics.2000
  • 2Lithgow T,Vandriol R,Bertram JF,et al.The protein product of the oncogene Bcl-2 is a component of the nuclear envelope, the endoplasmic reticulum, and the outer mitochondrial membrane[].Cell Growth and Differentiation.1994
  • 3Clark RSB,Cken J,Watkons SC,et al.A poptosis-suppressor gene Bcl-2 expression after traumatic brain injury in rats[].J Neurosur.1997
  • 4Nakamura M,Raghupathi R,Merry DE et al.Overexpression of Bcl-2 is neuropprotective after experimental brain injury in transgemc mice[].Journal of Comparative Neurology.1999
  • 5Chen DF,Schneider GE,Martinou JG,et al.Bcl-2 promotes regeneration of severed axons in mammalian CNS[].Nature.1997
  • 6Gonzalez-Garcia M,Garcia I,Ding L,et al.Bcl-x is expressed in embryonic and postnatal neural tissues and functions to prevent neuronal cell dearth[].Proceedings of the National Academy of Sciences of the United States of America.1995
  • 7Fiskum G.Mitochondrial participation in ischemic and traumatic neuronal cell death[].Journal of Neurotrauma.2000
  • 8Zhong LT,Sarafian T,Kane DJ,et al.Bcl-2 inhibits death of central neural cells induced by multiple agents[].Proceedings of the National Academy of Sciences of the United States of America.1993
  • 9Raghoupathi R,Fernaandez SC,Mural H,et al.Bcl-2 over expression attenuates cortical cell loss after traumatic brain injury in transgenic mice[].Journal of Cerebral Blood Flow and Metabolism.1998
  • 10Shimizu S,Eguchi Y,Kosaka H,et al.Prevention of hypoxia-induced cell death Bcl-2 and Bcl-x1[].Nature.1995

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