CAJ | 학술논문

目的探讨Che-1在创伤性脑损伤后大鼠皮质的表达变化及其与神经元凋亡和轴突再生的关系.方法 64只雄性SD大鼠按随机数字表法分为正常组、假手术组和外伤组,其中外伤组又分为12 h、1d、3d、5d、7d、14d6个时相组,每组8只.建立CCI颅脑损伤模型,使用Western印迹、免疫组化、免疫荧光、TUNEL标记等方法检测Che-1表达变化,神经元凋亡,p53、Bax、active-caspase-3、GAP43的表达变化及与Che-1的定位关系.结果相比较于正常组和假手术组,外伤后Che-1表达量增加,其蛋白表达量于损伤后第3天达到峰值(0.817 ±0.022,P＜0.05),且与神经元凋亡和轴突再生相关.p53、Bax、active-caspase-3、GAP43在外伤后的表达变化与Che-1存在时间和定位相关性.结论创伤性脑损伤后Che-1表达增加,且通过p53参与外伤后神经元凋亡与轴突再生.
목적 탐토Che-1재창상성뇌손상후대서피질적표체변화급기여신경원조망화축돌재생적관계.방법 64지웅성SD대서안수궤수자표법분위정상조、가수술조화외상조,기중외상조우분위12 h、1d、3d、5d、7d、14d6개시상조,매조8지.건립CCI로뇌손상모형,사용Western인적、면역조화、면역형광、TUNEL표기등방법검측Che-1표체변화,신경원조망,p53、Bax、active-caspase-3、GAP43적표체변화급여Che-1적정위관계.결과 상비교우정상조화가수술조,외상후Che-1표체량증가,기단백표체량우손상후제3천체도봉치(0.817 ±0.022,P＜0.05),차여신경원조망화축돌재생상관.p53、Bax、active-caspase-3、GAP43재외상후적표체변화여Che-1존재시간화정위상관성.결론 창상성뇌손상후Che-1표체증가,차통과p53삼여외상후신경원조망여축돌재생.
Objective To explore the altered expressions of Che-1 in rat brain cortex and relative biological functions after traumatic brain injury.Methods According to a random number table,a total of 64 male Sprague-Dawley rats were divided into normal,sham and trauma group.Then the trauma group was further divided into 6 phase sub-groups (12 h,1 d,3 d,5 d,7 d,14 d) (n =8 each).The craniocerebral injury (CCI) model was established to induce brain trauma at different timepoints.The examinations of Western blot and immunohistochemistry were performed to detect the expressions and diffusion changes of Che-1.Meanwhile the method of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) was employed to examine neuronal apoptosis.Additionally,the association of Che-1 with p53,active-caspase-3 and GAP43 was tested with Western blot and immunofluorescent staining.Results Compared with the normal and sham groups,the expression of Che-1 peaked at Day 3 post-injury (0.817 ± 0.022,P ＜ 0.05) and it was related with neuronal apoptosis.Moreover,the altered expressions of p53,GAP43 and active-caspase-3 were associated with the level of Che-1.Conclusion The expression of Che-1 is elevated after brain trauma and may be involved in neuronal apoptosis and axonal regeneration through p53.