高压氧对脑外伤大鼠海马神经元凋亡的影响

The effect of hyperbaric oxygen therapy on apoptosis:Expression of Bcl-2 and Bax protein in rats with traumatic brain injury

目的研究高压氧对于脑外伤大鼠神经细胞凋亡的作用。方法采用改进的Feency自由落体法建立脑外伤模型,72只大鼠随机分为正常对照组、脑外伤组、高压氧治疗组。在预定时间点采用TUNEL法和免疫组化法观察3组细胞的凋亡及Bcl-2和Bax蛋白表达情况。结果高压氧治疗组伤后第1,7,24天细胞凋亡率均低于脑外伤组。各时间点Bcl-2染色阳性细胞率均高于脑外伤组,各时间点Bax染色阳性细胞率均低于脑外伤组。结论高压氧可明显提高Bcl-2的表达,抑制Bax的表达,进而抑制细胞凋亡。

Objective To study the effects of hyperbaric oxygen therapy on traumatized cerebral neurons and investigate its mechanism in attenuating cerebral damage. Methods Seventy-two rats were randomly assigned to a control group, a traumatic brain injury group or a traumatic brain injury group treated with hyperbaric oxygen. Each group was observed 1 , 7 and 24 days after the operation. TUNEL was used to examine the distribution of apoptosis cells. An immunohistochemical method was used to examine the distribution of Bcl-2 and Bax immunoreactivepositive cells in the brain tissues. Results The average percentages of both apoptosis cells and Bcl-2 immunoreacrive-positive cells were lower in the CA1 region of the traumatized brains treated with hyperbaric oxygen than in those of the traumatic injury group at each time of observation. A significant difference in Bax immunoreactive-positive cells between the two groups was also observed. Conclusion Hyperbaric oxygen therapy can significantly protect neurons against traumatic brain injury and modulate the expression of the apoptosis related genes Bcl-2 and Bax, This may explain the protective mechanisms of hyperbaric oxygen therapy in treating traumatic brain injury.