摘要
目的研究脊髓压迫性损伤（compressedspinalcordinjury，CSCI）后脱髓鞘病变与半胱氨酸天冬氨酸蛋白酶-12（caspase-12）表达变化之间的关系，探讨CSCI后脱髓鞘病变机制。方法成年SD大鼠75只，按随机数字表法分为5组：正常组、对照组、压迫1d组、3d组、7d组，每组15只。采用自行设计制作的脊髓压迫模型，通过电镜和TUNEL染色、免疫荧光双标分别检测各组CSCI后神经纤维脱髓鞘的超微结构以及少突胶质细胞凋亡情况；运用免疫印迹技术检测与细胞凋亡有关的caspase-12表达。结果CSCI后神经纤维出现脱髓鞘病变，并随着压迫时间延长而逐渐加重；脊髓损伤后出现少突胶质细胞凋亡，压迫7d组与正常组相比，差异有统计学意义（P〈0．05）。caspase-12表达也随压迫时间延长而上调。结论caspase-12介导了少突胶质细胞凋亡，是CSCI后神经纤维脱髓鞘病变的机制之一。
Objective To investigate correlation between demyelination and caspase-12 expression alteration after compressed spinal cord injury （CSCI） so as to discuss mechanism of demyelinating lesion after CSCI. Methods Seventy-five adult SD rats were randomly divided into five groups, ie, normal group, control group, compression 1 d, 3 d and 7 d groups, with 15 rats per group. Models of spinal cord compression were established with a self-made device. Uhrastructure of the demyelinated nerve fibers was observed by electronic microscope and oligodendroeyte apoptosis was detected by TUNEL staining and double labeling immunofluorescence. Immunoblotting was used to defect caspase-12 that was related to cell apoptosis. Results Demyelination of nerve fiber occurred after CSCI and was aggravated with time. Apoptosis of oligodendrocytes was found after CSCI, and showed significant difference between compression 7 d group and normal group （ P 〈 0. 05 ）. Caspase-12 was also up- regulated with extension of compression time. Conclusion Caspase-12 mediating oligodendrocyte apoptosis is one of the mechanisms of nerve fiber demyelination after CSCI.
出处
《中华创伤杂志》
CAS
CSCD
北大核心
2013年第2期160-164,共5页
Chinese Journal of Trauma
基金
国家自然科学基金资助项目（30270437）
重庆市自然科学基金资助项目（cstc2012jjA10020）
重庆市卫生局中医药科技资助项目（2012-2-138）
重庆市教委科学技术研究资助项目（KJ120312）
重庆市渝中区科技计划资助项目（20110316）
