大鼠颅脑创伤后脑红蛋白的动态变化及对神经元的保护作用

发布时间：2018-06-21 01:11

本文选题：颅脑创伤 + 脑红蛋白　；参考：《中国老年学杂志》2016年21期

【摘要】：目的探讨颅脑创伤后脑红蛋白(NGB)动态变化及其神经保护作用。方法构建大鼠颅脑创伤模型,在大鼠颅脑创伤后0.5、1、3、6、12、24、48、72、96 h取大鼠脑组织,免疫组化观察各时间点大鼠脑组织中NGB、Bax和Bcl-2的动态变化,计算Bax/Bcl-2比值的动态变化。结果成功构建了大鼠颅脑创伤模型,大鼠脑组织中皮质神经元中NGB的含量较多,大鼠在颅脑损伤后NGB的表达水平急剧上升,在损伤后3 h脑组织中的NGB的表达水平达到高峰,随后出现缓慢下降;损伤后72 h NGB的表达出现又一高峰,之后下降;96 h时NGB的表达水平仍然高于对照组。大鼠颅脑创伤后3 h,皮质神经元中Bcl-2的表达水平达到高峰,随后开始缓慢下降;在创伤后24 h,Bcl-2的表达水平又出现一个高峰,之后开始逐渐下降;创伤后96 h皮质神经元中Bcl-2的表达水平仍然高于对照组。大鼠颅脑创伤后,皮质神经元中Bax的表达量急剧上升,在大鼠颅脑创伤后3 h,皮质神经元中Bax的表达水平达到高峰,之后逐渐下降;在48 h时Bax的表达量稍有升高,后又开始缓慢下降;创伤后96 h皮质神经元中Bax的表达水平仍然高于对照组。大鼠颅脑创伤后Bax/Bcl-2比值迅速增加,在创伤后6 h出现高峰,之后逐渐下降;在48 h时又出现缓慢增加,之后又逐渐下降;在创伤后96 h,Bax/Bcl-2的比值与对照组差异不显著(P0.05)。结论大鼠颅脑创伤后脑红蛋白表达增多,可以拮抗神经元细胞的凋亡,起到保护神经的作用。
[Abstract]:Objective to investigate the dynamic changes of NGB and its neuroprotective effect after traumatic brain injury. Methods the rat model of traumatic brain injury was established. The brain tissue was taken from the rat brain tissue at 0. 5 minutes after traumatic brain injury. The dynamic changes of NGB- Bax and Bcl-2 were observed by immunohistochemistry and the dynamic changes of the ratio of Bax / Bcl 2 were calculated. Results the rat model of craniocerebral trauma was successfully established. The content of NGB in the cortex neurons of the rats was higher than that in the control group, and the expression level of NGB increased sharply after brain injury, and reached the peak at 3 h after brain injury. After 72 hours of injury, the expression of NGB appeared another peak, then decreased at 96 h, the expression level of NGB was still higher than that of the control group. After traumatic brain injury, the expression of Bcl-2 reached its peak at 3 hours after traumatic brain injury, then began to decrease slowly, and the expression level of Bcl-2 appeared a peak at 24 hours after traumatic brain injury, and then decreased gradually. The expression of Bcl-2 in cortical neurons at 96 h after trauma was still higher than that in control group. After craniocerebral trauma, the expression of Bax in cortical neurons increased sharply, reached a peak at 3 h after traumatic brain injury, then decreased gradually, and increased slightly at 48 h. The expression of Bax in cortical neurons at 96 h after trauma was still higher than that in the control group. After traumatic brain injury, the ratio of Bax / Bcl-2 increased rapidly, peaked at 6 h after trauma, then decreased gradually, increased slowly at 48 h, then decreased gradually, and had no significant difference from the control group at 96 h after trauma (P 0.05). Conclusion the increased expression of brain erythroprotein after traumatic brain injury can antagonize the apoptosis of neuronal cells and protect the nerve.
【作者单位】：浙江大学医学院附属第四医院急诊科;义乌稠州医院;金华中心医院急诊科;
【基金】：浙江省医药卫生科技计划项目(2014KYA177)
【分类号】：R651.15

【相似文献】