高压氧治疗模型大鼠颅脑损伤性神经功能障碍的研究

Study of craniocerebral injury in rats with hyperbaric oxygen therapy

目的:研究模型大鼠颅脑损伤后高压氧治疗神经功能障碍的作用并讨论其意义。方法:成年健康SD大鼠用改良自由落体方法制备脑损伤模型36只,随机分为假手术组、颅脑损伤组和高压氧组,每组12只。研究大鼠在损伤后7、14和28 d用改良神经功能缺损评分(MNSS)评价神经功能,结果经统计学处理。结果:颅脑损伤组和高压氧组大鼠在损伤后7、14和28 d神经功能缺损评分均升高(P<0.01)。与假手术组比较,颅脑损伤组和高压氧组神经功能缺损评分升高(P<0.01),同时高压氧组评分显著低于颅脑损伤组(P<0.01)。与假手术组比较,各个时间点颅脑损伤组和高压氧组大鼠神经细胞凋亡数明显减少(P<0.01);与颅脑损伤组比较,高压氧组大鼠损伤7、14和28 d各时间点的神经细胞凋亡数也明显减少(P<0.05)。结论:高压氧能促进颅脑损伤大鼠神经功能缺损的恢复,同时降低神经细胞凋亡作用。这为应用高压氧治疗颅脑损伤提供依据,也为研究Notch信号调控神经再生机制提供参考。

Objective：To study the effect of hyperbaric oxygen therapy on neural dysfunction in rats after brain injury and to discuss its significance.Methods：Adult healthy 36 SD rats were randomly divided into sham operation,craniocerebral injury and hyperbaric oxygen groups,12 rats in each group.The neurological function of rats was evaluated by Modified Neurological Severity Scores（MNSS） at 7,14 and 28 d after injury,and the results were statistically analyzed.Results：In the brain injury group and the hyperbaric oxygen group,at 7,14 and 28 d the scores of nerve function defect were all increased after the injury（P〈0.01）.Compared with sham operation group,the neurological deficit score in craniocerebral injury group and hyperbaric oxygen group increased（P〈0.01）,while the score of hyperbaric oxygen group was significantly lower than that in craniocerebral injury group（P〈0.01）.Compared with the sham operation group,the number of neuron apoptosis in the craniocerebral injury group and hyperbaric oxygen group decreased significantly（P〈0.01） at each time point.Compared with the craniocerebral injury group,the number of neuron apoptosis in the hyperbaric oxygen group at 7,14 and 28 d on each time point was also significantly reduced（P〈0.05）.Conclusion：The results show that hyperbaric oxygen can promote the recovery of neural function defect and decrease the apoptosis of neurons in the brain injury rats.This provides a basis for the application of hyperbaric oxygen in the treatment of craniocerebral injury,and also provides a reference for the study of the mechanism of Notch signal regulation of nerve regeneration.