摘要
目的观察吡哆醇诱导的感觉神经元病大鼠在坐骨神经挤压伤后神经再生相关蛋白的表达水平,探讨神经元分子微环境变化对神经再生修复的重要意义。方法制作吡哆醇诱导的感觉神经元病模型,在此基础上制作双侧坐骨神经挤压伤模型。观察神经挤压损伤后7、14、21和28d大鼠的背根神经节TUNEL标记阳性细胞百分比变化;利用蛋白印迹技术,观察神经再生相关蛋白(GAP-43)和神经生长因子受体(trkA)表达水平变化。结果背根神经节细胞早期有较多的TUNEL标记细胞,但21～28d由于大部分细胞变性坏死,TUNEL标记细胞反而减少。背根神经节细胞GAP-43和trkA蛋白有一定水平的表达,但总体水平低于单纯坐骨神经损伤时。结论中毒造成的感觉神经节病变危及神经元的生存,导致基因表达体系不完整,使损伤神经的再生修复能力下降。
Objective To evaluate the significance of molecular mieroenvironment in neurons for the nerve regeneration and repair by investigating the dynamic changes of nerve regrowth-associated proteins following bilateral sciatic nerves crush in pyridoxine-induced ganglionopathy rats model. Methods Bilateral sciatic nerve crush were performed 4 weeks after induction of pyridoxine-induced ganglionopathy. The changes of mean percentage of TUNEL positive cells in dorsal root ganglion （DRG） following bilateral sciatic nerves crush for 7 days, 14 days, 21 days, and 28 days. Western blotting techniques were used to investigate the expression of GAP- 43 and trk A in different duration following sciatic nerve crush injury. Results The percentage of TUNEL positive neurons in DRG significantly increased in early stage and markedly decreased in 21-28 days after sciatic nerve crush. The expression of GAP 43 and trk A in DRG were upregulated at all time point after nerve injury in pyridoxine induced ganglionopathy, but the overall level was lower than that of pure nerve crush injury. Conclusion In pyridoxine-induced ganglionopathy, neurons in DRG undergo survival crisis, the gene expression system was disintegrated, the capacity to regenerate their axons declines after nerve injury.
出处
《中国康复理论与实践》
CSCD
2009年第8期732-735,共4页
Chinese Journal of Rehabilitation Theory and Practice
基金
北京市教委科技发展计划资金资助项目(KM200610025020)
