You Position: Home > Paper
Inhibitory effect of chondroitinase ABC on ephrin A4 expression after spinal cord injury in rats
( views:44, downloads:0 )
- Author:
- No author available
- Journal Title:
- Acta Physiologica Sinica
- Issue:
- 6
- DOI:
- No doi available
- Key Word:
- 脊髓损伤;硫酸软骨素酶ABC;酪氨酸蛋白激酶A4
Abstract： 本研究旨在探讨大鼠脊髓损伤(spinal cord impairment,SCI)后硫酸软骨素酶ABC (chondroitinase ABC,ChABC)对酪氨酸蛋白激酶A4 (ephrin A4,EphA4)表达变化的影响.选取成年雌性SD大鼠,随机分为假手术组、生理盐水(NS)组和ChABC组.NS组和ChABC组大鼠行脊髓半切损伤术,并通过蛛网膜下腔分别注射NS和ChABC;假手术组仅接受背部切开术,没有半切脊髓.SCI后1、3、7、14、21 d取损伤段脊髓样品,采用免疫荧光染色和免疫印迹检测各组EphA4表达；SCI后3d采用免疫荧光双标法检测损伤段脊髓内生长相关蛋白-43 (growth associated protein 43,GAP-43)和胶质纤维酸性蛋白(glial fibrillary acidic protein,GFAP)的表达情况.结果显示,术后1、3、7d,NS组EphA4阳性神经元数明显少于假手术组(P＜0.01),而术后14、21 d,ChABC组和NS组EphA4阳性神经元多于假手术组(P＜0.05).值得注意的是,在术后各时间点,ChABC组EphA4阳性神经元数均明显低于NS组(P＜0.01).免疫印迹结果与免疫荧光术所得结果一致.术后3d,各组GFAP标记胶质细胞数之间相比较,假手术组最多,NS组次之,ChABC组最少；另外,各组均未出现GAP-43阳性神经元.以上结果提示,SCI后,ChABC可以降低神经元EphA4的表达,并减少EphA4阳性神经元周围的胶质细胞数,从而改善脊髓的内环境,有利于神经轴突的生长与延伸.
- [1]黄纯海,李学军,黄军,等.大鼠脊髓全横断损伤模型的建立[J].2008,(2).
- [2]张红,刘维钢,黄瑾,等.大鼠脊髓完全性损伤模型的建立[J].2009,(33).
- [3]张德盛,钟德君,宋跃明,等.硫酸软骨素酶ABC-聚乳酸-聚乙醇酸共聚物缓释微球的制备及其体外性质[J].2008,(32).
- [4]赵燕玲,张博爱,贾延劼,等.EphA4在海人酸诱导大鼠大脑皮层神经元凋亡中的表达及天麻素的影响[J].2009,(10).
- [5]Bouvier D,Pasquale EB,Tremblay ME,etc.Localization of EphA4 in axon terminals and dendritic spines of adult rat hippocampus.[J].2007,501(5).
- [6]Claire M, Edwards,Gregory R, Mundy.Eph receptors and ephrin signaling pathways: a role in bone homeostasis.[J].2008,5(5).
- [7]M E, Martone,J A, Holash,A, Bayardo,etc.Immunolocalization of the receptor tyrosine kinase EphA4 in the adult rat central nervous system.[J].1997,771(2).
- [8]Greferath U,Canty AJ,Murphy M,etc.Eph tyrosine kinase receptor EphA4 is required for the topographic mapping of the corticospinal tract[J].2006,103(42).
- [9]Riad M,Murai KK,Pasquale EB,etc.Pre-synaptic and post-synaptic localization of EphA4 and EphB2 in adult mouse forebrain.[J].2008,106(2).
- [10]Rogers RC,Beattie MS,Bresnahan JC,etc.Cell death in models of spinal cord injury.[J].2002,137(0).
- [11]McLenachan S,Turnley A,Goldshmit Y.Roles of Eph receptors and ephrins in the normal and damaged adult CNS.[J].2006,52(2).
- [12]Nobuhiko, Yamamoto.[Molecular mechanisms of thalamocortical circuit formation].[J].2008,60(4).
- [13]Doller C,Goucher DR,Silver J,etc.Robust regeneration of adult sensory axons in degenerating white matter of the adult rat spinal cord.[J].1999,19(14).
- [14]M E, Schwab,P, Caroni.Oligodendrocytes and CNS myelin are nonpermissive substrates for neurite growth and fibroblast spreading in vitro.[J].1988,8(7).
- [15]Pasquale EB.Eph-ephrin bidirectional signaling in physiology and disease[J].2008,133(1).
- [16]Rhodes KE,Fawcett JW.Chondroitin sulphate proteoglycans: preventing plasticity or protecting the CNS?[J].2004,204(1).
- [17]Romanovsky AA,Ivanov AI.Putative dual role of ephrin-Eph receptor interactions in inflammation[J].2006,58(7).
- [18]Ikegami T,Takahashi T,Okada S,etc.Chondroitinase ABC combined with neural stem/progenitor cell transplantation enhances graft cell migration and outgrowth of growth-associated protein-43-positive fibers after rat spinal cord injury.[J].2005,22(12).
- [19]Grados Munro EM,Fournier AE.Myelin-associated inhibitors of axon regeneration.[J].2003,74(4).
- [20]Wandosell F,Moreno Flores-MT.Up-regulation of Eph tyrosine kinase receptors after excitotoxic injury in adult hippocampus.[J].1999,91(1).
- [21]Higuchi H,nat2.med.osaka-u.ac.jp,Tohyama M,etc.The p75 receptor transduces the signal from myelin-associated glycoprotein to Rho.[J].2002,157(4).
- [22]A W, Boyd,M, Lackmann.Signals from Eph and ephrin proteins: a developmental tool kit.[J].2001,2001(112).