纳洛酮对颅脑损伤后细胞凋亡的Caspase-3介导的信号传递机制的实验研究

目的观察纳洛酮对严重颅脑损伤后神经细胞Caspase-3表达的影响,探讨Caspase-3介导的信号传递机制.方法选用家兔77只,随机分成正常组、对照组、大剂量组和小剂量组,分别予非颅脑损伤、颅脑损伤、颅脑损伤后大剂量纳洛酮腹腔注射及颅脑损伤后小剂量纳洛酮腹腔注射处理,15天后均断头处死,于致伤处和对侧处取材,采用SP法制作切片,观察比较各组神经细胞Caspase-3表达阳性细胞数量.结果致伤处或对侧处,正常组、大剂量组、小剂量组和对照组神经细胞Caspase-3表达阳性细胞数量两两之间比较均有显著差异,值从小到大均为:正常组＜大剂量组＜小剂量组＜对照组.结论Caspase-3介导的信号传递机制可能参与纳洛酮抗颅脑损伤后神经细胞的凋亡过程.

The experimental study on caspase-3 mediated signal transfer mechanism in the anti-apoptosis of naloxone in experimental severe brain injury

Objective To explore caspase-3 mediated signal transfer mechanism of the anti-apoptosis of naloxone to experimental severe traumatic brain tissue. Methods 77 rabbits were randomly divided into normal group with no craniocerebral injury, control group with craniocerebral injury, high dose group with and small dose group with intraperitoneal administration of naloxone after brain trauma, were decapitated in 15days, and histopathology studies of SP were made, and the number of caspase-3 positive cells were observed and the differences among the values of each group respectively were compared. Results The differences among the number of caspase-3 positive cells in each group were found very apparently, they were ranged from the least to the most values: normal group, high dose group, small dose group and control group. Conclusion It is suggested that the signal transfer mechanism with involvement of caspase-3 has participated in the anti-apoptosis of naloxone to severe traumatic nervous cells