摘要
目的探究单唾液酸四己糖神经节苷脂(monosialoganglioside,GM1)对大鼠急性脑损伤的保护作用及相关机制。方法采用落体撞击法使大鼠左顶叶形成局部性脑挫裂伤。将65只SD大鼠随机分为假手术组(n=5)、脑损伤组(n=30)和GM1组(n=30),分别在造模给药后3、7、14、28、56、168 h时,每次各组随机选取5只(假手术组为1只),通过免疫组化染色检测脑组织Bcl-2、Bax的蛋白表达以及PARP降解情况,TUNEL法观察神经细胞凋亡的情况。结果脑损伤组各时间点Bax、Bcl-2蛋白表达与假手术组比较差异有统计学意义(P<0.05),GM1组各时间点Bax、Bcl-2蛋白表达与脑损伤组比较差异有统计学意义(P<0.05),且GM1组在14 h后Bax、Bcl-2蛋白表达与假手术组差异无统计学意义。给药后Bax/Bcl-2比值有所下降,在14 h下降最为明显。脑损伤组PARP降解及细胞凋亡率在各时间点显著高于假手术组(P<0.05),GM1组PARP降解在28、56、168 h显著低于脑损伤组(P<0.05),神经细胞凋亡率在各时间点显著低于脑损伤组(P<0.05)。结论神经节苷脂GM1能够降低急性脑损伤大鼠Bax/Bcl-2比值,同时PARP降解缓解,凋亡细胞减少。
Objective To explore the protective effect of monosialoganglioside（ GM1） on rats with acute brain trauma and its relevant mechanism.Methods Localized brain contusion model in rats were constructed by Feeney＇s method. 65 SD rats were randomly divided into three groups： shamoperation group（ n = 5）,brain injury group（ n = 30） and GM1 group（ n = 30）. The rats were killed at 3,7,14,28,56,168 h after administration,5 rats in each group（ 1 rats in sham-operation group）. Bax and Bcl-2 protein expression and PARP were decected by immunohistochemical method. The neuronal apotosis was detected by TUNEL. Results There were significant differences in expression of Bax and Bcl-2 protein between brain injury group and sham-operation group at each time point（ P〈0. 05）. There were significant differences in expression of Bax and Bcl-2 protein between GM1 group and brain injury group at each time point（ P〈0. 05）,while there were no significant differences in expression of Bax and Bcl-2 protein after 14 h between GM1 group and sham-operation group. After administration,the Bax / Bcl-2 values decreased and was obvious at 14 h. Degradation of PARP and rate of neuronal apotosis in brain injury group at each time point were significantly higher than those in sham-operation group（ P〈0. 05）. Degradation of PARP in GM1 group at 28 h,56 h,168 h were significant lower than those in brain injury group（ P〈0. 05）,and rate of neuronal apotosis was lower at each time point than those in brain injury group（ P〈0. 05）. Conclusion GM1 could reduce value of Bax / Bcl-2,degradation of PARP and apoptosis in rats with traumatic injury brain.
出处
《中国生化药物杂志》
CAS
2015年第9期48-50,共3页
Chinese Journal of Biochemical Pharmaceutics
基金
国家自然科学基金(81171147)
