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外源性BDNF对急性高眼压后大鼠视网膜ERK1/2磷酸化的影响 被引量:3

The expression of p-ERK1/2 receptor in rat retina following acute high intraocular pressure with BDNF pre-treated
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摘要 为研究脑源性神经生长因子(BDNF)干预对急性高眼压后大鼠视网膜磷酸化的细胞外信号调节激酶(p-ERK1/2)表达变化的影响,本实验将成年大鼠随机分为单纯高眼压组、BDNF预处理高眼压组和溶媒预处理高眼压组,BDNF预处理高眼压组和溶媒预处理高眼压组动物左眼于加压前2d分别给予BDNF或溶媒预处理,右眼设为正常对照。各组动物左眼眼压升高至闪光视网膜电图b波消失的临界眼压并维持60min,动物分别存活1、3、7、14d后处死,冰冻切片行p-ERK的免疫组织化学染色。结果显示与正常对照相比,单纯高眼压组急性高眼压后p-ERK表达下调(P<0.05),1、3、7d组内核层出现p-ERK阳性细胞;溶媒预处理高眼压组实验结果与单纯急性高眼压组相似;BDNF预处理高眼压组急性高眼压后1、3、7d时p-ERK的表达与正常对照组相似,7d和14d出现了重新分布。此结果提示外源性BDNF可能通过促进急性高眼压后视网膜ERK1/2的活化对受损的视网膜起保护作用。 To investigate the expression of phospho-extracellular signal - regulated kinase 1/2 (p-ERK1/2) in rat retina following acute high intraocular pressure(HIOP) with brain-derived neuretrophic factor (BDNF) pre-treated. Seventy-two adult rats were randomly divid- ed into acute HIOP group, BDNF pre-treated HIOP group and vehicle pre-treated HIOP group. The left eyes of rats in BDNF pre-treated HIOP group and vehicle pre-treated HIOP group were injected with BDNF or vehicle respectively 2 days before HIOP. The intraocular pressure of all left eyes was increased until b wave of flash electroretinogragh disappeared and such pressure maintained for 60 min. All the right eyes were served as normal control group. The rats were sacrificed after 1, 3, 7 or 14 days, immunohistochemistry for detecting the expression of p-ERK1/2 was used. The results showed that compared to the normal control group, the expression of p-ERK1/2 was decreased significandy (P 〈 0.05 )during reperfusion in the acute HIOP group, and we could detect p-ERK1/2 positive cells in the inner nuclear layer of 1,3 and 7 day groups. The expression of p-ERK1/2 during reperfusion in vehicle control group was similar to those in acute HIOP group. In the BDNF pre-treated HIOP group, the expression of p-ERK1/2 was similar to the normal group at 1,3 and 7 day follow- ing HIOP, but at 7 and 14 day group, there are p-ERK1/2 positive cells appears in the inner nuclear layer. These results indicate that the protective function of exogenous BDNF to injured retina may be involved in promoting the phosphorylation of ERK1/2 the retina.
出处 《神经解剖学杂志》 CAS CSCD 北大核心 2008年第5期492-495,共4页 Chinese Journal of Neuroanatomy
基金 国家自然科学基金(Nos30100098,30570979)资助项目
关键词 急性高眼压 BDNF P-ERK1/2 RGCS acute high intraocular pressure, BDNF, p-ERK1/2, RGCs
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参考文献9

  • 1黄菊芳,蒋丽珠,童建斌,陈旦,熊鲲,曾乐平.脑源性神经营养因子预处理后急性高眼压下大鼠视网膜TrkB的表达变化[J].解剖学杂志,2006,29(6):734-737. 被引量:7
  • 2熊鲲,黄菊芳,童建斌,陈旦,潘爱华,罗学港.急性大鼠眼高压诱导的不同缺血/再灌内层视网膜的变化[J].解剖学杂志,2005,28(1):46-49. 被引量:21
  • 3Chen Z, Gibson TB, Robinson F et al. Map kinases. Chem Rev, 2001 ; 101:2449 - 2476.
  • 4Newman E, Reichenbaeh A. Themuller cell: A functional element of the retina. Trends Neurosci, 1996 ;19:307 - 312.
  • 5黄菊芳,童建斌,刘求理,楚亚平,罗学港.急性高眼压后大鼠视网膜谷氨酰胺合成酶的表达变化[J].神经解剖学杂志,2004,20(6):548-552. 被引量:8
  • 6Taylor S, Srinivasan B, Wordinger RJ et al. Glutamate stimulates neurotrophin expression in cultured MUller cells. Brain Res Mol Brain Res, 2003 ; 111 : 189 - 197.
  • 7Roth S, Shaikh AR, Hennelly MM et al. Mitogen-activated protein kinases and retinal ischemia. Invest Ophthalmol Vis Sci, 2003 ; 44:5383 - 5395.
  • 8Akiyama H, Nakazawa T, Shimura Met al. Presence of mitogenactivated protein kinase in retinal Muller ceils and its neuroprotectire effect ischemia-repeffusion injury. Neuroreport, 2002; 13 : 2103 -2107.
  • 9Alessandrini A, Namura S, Moskowitz MA et al. MEK1 protein kinase inhibition protects against damage resulting from focal cerebral ischemia. Proc Natl Acad Sci USA, 1999 ;96 : 12866 - 12569.

二级参考文献30

  • 1Rosenbaum DM, Rosenbaum PS, Singh M, et al. Functional andmorphologic comparision of two methods to produce transient retinalischemia in the rat. J Neuro-ophthalomol, 2001, 21(1):62-68.
  • 2Villegas-Perez MP, Vidal-Sam M, Raminsky M, et al. Rapid andprotected phases of retinal ganglion cdll loss follow axotomy in thenerve of adult rats. J Neurobiol, 1993, 24(1):23-36.
  • 3Barnett NL, Osborne NN. Prolonged bilateral carotid artery occlu-sion induces electrophysiologieal and immunohistochemical changes tothe rat retina without causing histological damage. Exp Eye Res,1995, 61(1) :83-90.
  • 4Osborne NN, Barnett NL. Redistribution of GABA immunoreactiv-ity following central retinal artery occlusion. Brain Res, 1995, 677(2) :337-340.
  • 5Ni Ho Park, Cozier F, Ong OC, et al. Induction of heat shock pro-tein 72 protects retinal ganglion cells in a rat glaucoma model. InvestOphthalmol Vis Sci, 2001, 42(7): 1522-1530.
  • 6LOK J, Martin LJ. Rapid subcellular redistribution of Bax precedescaspase-3 and endonuclease activation during excitotoxic neuronalapoptosis in rat brain. J Neurotrauma, 2002, 19(7):815-828.
  • 7Chen H, Weber AJ. Expression of glial fibrillary acidic protein andglutamine synthestase by muller cells after optic nerve damage andintravitreal application of BDNF. Glia, 2002,38(2): 115-125.
  • 8Quigley HA, Nickells RW, Kerrigan LA, et al. Retinal ganglion celldeath in experimental glaucoma and after axotomy occurs by apopto-sis. Invest Ophthalmol Vis Sci, 1995, 36(5):774-786.
  • 9Cheon EW, Park CH, Kang SS, et al. Change in endothelial nitric ox-ide synthase in the rat retina following transient ischemia. Neurore-port, 2003,14 (3): 329-333.
  • 10Napper GA, Pianta M J, Kalloniatis M. Reduced glutamate uptake by retinal glial cells under ischemic/hypoxic condition. J Vis Neurosci, 1999; 16 : 149- 160

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