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酪氨酸受体激酶B在胚胎脊髓修复成鼠损伤脊髓过程中的变化
引用本文:李兵仓,王正国,朱佩芳,胡建,李应玉,廖维宏. 酪氨酸受体激酶B在胚胎脊髓修复成鼠损伤脊髓过程中的变化[J]. 中华创伤杂志, 1998, 14(5): 270-273
作者姓名:李兵仓  王正国  朱佩芳  胡建  李应玉  廖维宏
作者单位:第三军医大学附属大坪医院、野战外科研究所
摘    要:目的确定酪氨酸受体激酶B(trkB)在胚胎脊髓修复成鼠脊髓损伤过程中的变化。方法将妊娠14天胚胎脊髓植入急性损伤的成体脊髓后1,3,5,7,10,15和30天,用原位杂交、斑点杂交和免疫组化技术对trkBmRNA与蛋白作定性和定量观察。结果定性观察表明,在正常大鼠脊髓内,trkBmRNA杂交产物主要分布在神经元和胶质细胞,神经纤维杂交反应不明显;脊髓损伤后阳性神经元和胶质细胞都有所增加,但阳性神经纤维增加的数目略为突出;胚胎脊髓植入损伤脊髓后,上述各阳性反应成分进一步增加,尤其是阳性神经纤维的增加更为显著。定量观察显示的trkBmRNA的分子杂交反应与定性观察结果大体一致。免疫组化显色的trkB蛋白,无论分布还是反应强度都与其mRNA的变化大致相符。结论损伤脊髓在移植修复过程中能够以调整受体合成的方式来适应营养环境的变化,但胶质细胞受体合成增加可能起了与神经成分争夺神经营养因子的副作用

关 键 词:脊髓损伤  脊髓移植  酪氨酸受体激酶B

Changes of trkB During Embryonic Spinal Cord Repairing Spinal Cord Injury in Adult Rats
LI Bing cang,WANG Zheng guo,ZHU Pei fang,et al.. Changes of trkB During Embryonic Spinal Cord Repairing Spinal Cord Injury in Adult Rats[J]. Chinese Journal of Traumatology, 1998, 14(5): 270-273
Authors:LI Bing cang  WANG Zheng guo  ZHU Pei fang  et al.
Affiliation:LI Bing cang,WANG Zheng guo,ZHU Pei fang,et al. Research Institute of Surgery,Third Military Medical University,Chongqing 400042
Abstract:Aim To determine the changes of tyrosine receptor kinase B (trkB) during embryonic spinal cord repairing spinal cord injury in adult rats. Methods With the technique of molecular hybridization and immunohistochemistry, the changes of trkB mRNA and its protein were demonstrated qualitatively and quantitatively at days 1, 3, 5, 7, 10, 15 and 30 after embryonic spinal cord was transplanted into the acutely injured spinal cord of adult rats. Meanwhile, the normal rats and the rats with spinal cord injury but with no repair were used as the controls. Results It was shown qualitatively by in situ hybridization that the reaction products distributed mainly in the cytoplasm of neurons and gliocytes in the normal spinal cord, but the nerve fibres without distinctive products. Following spinal cord injury, the number of positively reacting elements mentioned above increased, but among them the nerve fibres increased even a little more. After the transplantation, all the positively hybridizing elements further increased in number, and the nerve fibers increased prominently, too. The quantitative determination on the intensity of in situ hybridization and dot hybridization showed similar changes as that of the qualitative observation. Not only intenseness but also distribution of trkB protein revealed by immunohistochemistry was basically coincident with that of trkB mRNA. Conclusion During the course of embryonic spinal cord repairing injured spinal cord, the host tissue can modulate synthesis of neurotrophine receptor and in this way make itself to be adapted to the changes of trophic enviroment. However, the increase of the receptor in gliocyte may result in a side effect of grabing neurotrophine with neurons and nerve fibres.
Keywords:Spinal cord injury Spinal cord transplantation Tyrosine receptor kinase B
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