摘要
目的观察实验性糖尿病大鼠在坐骨神经挤压伤后神经生长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。方法制作实验性糖尿病大鼠模型,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大鼠背根神经节TUNEL标记阳性细胞百分比变化;利用免疫组化和蛋白印迹技术(Western-blot),观察神经生长相关蛋白(GAP-43)和神经生长因子受体(trkA)表达水平变化。结果实验性糖尿病大鼠坐骨神经损伤后,所有时程背根神经节细胞均有较多的TUNEL标记细胞,但以14～21d显著;各时程背根神经节细胞GAP-43和trkA蛋白均有一定水平的表达,但其表达水平低于非糖尿病组。结论实验性糖尿病大鼠坐骨神经背根神经节存在凋亡应激,其神经再生相关基因表达体系不完整,对神经损伤的再生修复能力下降。
Objective To evaluate the significance of molecular microenvironment in neurons for nerve regeneration and repair by investigating the dynamic changes of nerve regrowth-assoeiated proteins following sciatic nerves crush in rats with streptozotocin-induced experimental diabetes. Methods Bilateral sciatic nerve crush was performed 4 weeks after induction of streptozotocin-induced experimental diabetes, the 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, were evaluated. Immunohistochemical staining and Western-blot techniques were used to investigate the expression of nerve growth associated protein （ GAP-43 ） and nerve growth factor receptor （ trk A ） in different duration following sciatic nerve crush injury. Results The percentage of TUNEL positive neurons in DRG significantly increased in all stages after sciatic nerve crush, reaching a peak at 14 -21 days. The expression of GAP-43 and trk A in DRG were upregulated at all time points after nerve injury in streptozotocin-induced experimental diabetes, but the overall level was lower than that of non-diabetic rats. Conclusion In streptozotocin-induced experimental diabetes, neurons in DRG undergo survival crisis, the nerve regrowth-associated gene expression system was disintegrated, the capacity to regenerate their axons declines after nerve injury.
出处
《首都医科大学学报》
CAS
北大核心
2009年第5期664-670,共7页
Journal of Capital Medical University
基金
北京市教育委员会科技发展计划(KM200610025020)资助项目~~
