期刊文献+

大鼠局造脑缺血预处理后c-Ret的表达

The present of c-RetmRNA after focal ischemic preconditioning in rat
下载PDF
导出
摘要 目的观察对比胶质细胞源性神经营养因子受体c-Ret在大鼠局造脑缺血预处理后和脑缺血后的表达。方法实验采用c-Ret原位杂交技术,观察胶质细胞源性神经营养因子受体c-Ret在成年大鼠脑皮质的表达。结果缺血周边区可见c-RetmRNA阳性表达的神经元,MCAO3h,缺血周边区阳性表达开始增多,与正常对照组相比差异具有显著性,P<0.05,PC+MCAO组与MCAO组无差异,P>0.05,PC+MCAO和MCAO组随时间延长,c-RetmRNA在缺血周边区表达增强,并在1d时出现高峰,随后表达减低。在6h、12h、1d时与MCAO组比较有显著性差异,P<0.05,在3d和7dIPC+MCAO组无差异性。反应产物在细胞内呈棕褐色,清晰可辨,对照组只有极少量表达。结论c-Ret在脑缺血预处理后表达增高,可能对缺血引起的神经损伤起到重要的保护作用。 Objective In order to investigate and compare the differences after focal ischemic preconditionlng(PC) and ischemic in rat brain. Methods the present study research the c-RetmRNA express intervent by IPC through hybridition in situ technique. Resuits the result show that there have thinness express in control and no in ischemic core area but high express in infarct border. Express local in survival and complete shape neuron but none in pyknosis and necrosis neuron. There have obviously difference with MCAO group at 6 h,12 h and ld in IPC + MCAO group but no express besides ischemic area and need indicate later. Conclusion c-Ret shown high present after focal ischemic preconditioning and may play an important role protect against neurological impairment.
出处 《中国实验诊断学》 2008年第7期832-835,共4页 Chinese Journal of Laboratory Diagnosis
关键词 胶质细胞源性神经营养因子受体c—Ret 脑缺血 预处理 大鼠 c-Ret ischemic preconditioning rat
  • 相关文献

参考文献17

  • 1Kitagawa K, Matsumoto M,Tagaya M, Hata R, Ueda H, Niinobe M, Handa N,Fukunaga R, Kimura K, Mikoshiba K, Kamada T "Ischemic tolerance" phenomenon found in the brain[J]. Brain Res. 1990,528:21.
  • 2Crespel A, Baldy-Moulinier M, Lemer Natoli M. Neurogenesis in the adult brain:the demise of a dogma and the advent of new treatments [J].Bey Neurol. 2004,160(12) : 1150.
  • 3Calabresi P, Centonze D, Pisani A, Cupini L, Bemardi G. Synaptie plasticity in the ischaemic brain. Lancet Neurol[ J]. 2003, (10):622.
  • 4Cre Allred RP,Jones TA. Unilateral ischemic sensorimotor cortical damage in female rats:forelimb behavioral effects and dendritic Structural plasticity in the contralateral homotopic cortex[ J]. Exp Neurol, 2004,190(2) : 433.
  • 5Schaller B, Andres RFI, Huber AW, Meyer M, Perez-Bouza A, Ducray AD, Seiler RW, Widmer HR. Effect of GDNF on differentiation of cultured ventral mesencephalic dopaminergic and non-dopaminergic calretinin-expressing neurons[J]. Brain Res,2005,1036(1 - 2) : 163.
  • 6Theodore J Price, Michael D Louria, Damaries Candelario-Soto. Treatment of trigeminal ganglion neurons in vitro with NGF, GDNF or BDNF: effects on neuronal survival, neurochemical properties and TRPV1-mediated neuropeptide secretion[J]. BMC Neuroscience,2005,10:1186.
  • 7Kashiba H, Uchida Y, Senba E. Distribution and colocalization of NGF and GDNF family ligand receptor mRNAs in dorsal root and nodose ganglion neurons of adult rats[J]. Mol Brain Res,2003,110:52.
  • 8Skoff AM, Resta C, Swamydas M, et al. Nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF) regulate substance P release in adult spinal sensory neurons [ J ]. Neurochem Res, 2003, 28:847. GDNF.
  • 9Chunnian Zhao, Karen Veltri, Songlin Li. NGF, BDNF,NT-3, and GDNF mRNA Expression in Rat Skeletal Muscle following Denervation and Sensory Protection [ J ]. Journal of Neurotrauma, 2004,21 ( 10 ) : 1468.
  • 10Dauer W, Przedborski S. Parkinson' s Disease: Mechanisms and Models [ J]. Neurons Vol, 2003,39: 889.

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