p38、CHOP和细胞凋亡相关因子Bcl-2、Bax在PTSD大鼠中缝背核的表达

Expression of p38,CHOP and Bcl-2,Bax of apoptosis related factors in the dorsal raphe nucleus of PTSD rats

目的从蛋白和基因水平上观察PTSD大鼠中缝背核神经元p38、CHOP和细胞凋亡相关因子Bcl-2、Bax的表达量变化。方法采用国际上公认的的单一延长应激(single-prolonged stress,SPS)的方法建立PTSD大鼠模型;采用Morris水迷宫测试SPS刺激后大鼠的空间记忆和学习能力;采用Western blot及Real Time PCR检测PTSD大鼠中缝背核神经元p38、CHOP和细胞凋亡相关因子Bcl-2、Bax的蛋白及mRNA水平表达。结果模型组大鼠平均逃避潜伏期显著高于正常对照组,而在目标象限停留的时间百分比明显低于正常对照组。SPS刺激后,PTSD大鼠中缝背核神经元p38、CHOP和细胞凋亡相关因子Bcl-2、Bax在蛋白和基因水平阳性表达比正常对照组增多。结论 SPS刺激使PTSD大鼠中缝背核神经元的p38-CHOP细胞凋亡信号通路激活,诱发了下游的级联反应,导致了中缝背核神经元的凋亡。

Objective To observe the changes of p38, CHOP, Bcl-2 and Bax proteins and gene in the dorsal raphe nucleus of PTSD rats. Methods The PTSD rat model was established using the single-prolonged stress （SPS） method. The spatial memory and learning ability of the rats were measured by Morris water maze. Western blot and Real Time PCR were used to detect the protein and mRNA expression of p38, CHOP, Bcl-2 and Bax in the dorsal raphe nucleus of PTSD rats. Results The mean escape latency was significantly higher in model rats than in the normal control group, but the percentage of time spent in the target quadrant was significantly lower in model rats than in the normal control group. The protein and gene expression levels of p38, CHOP, Bcl-2 and Bax in the dorsal raphe nucleus were increased in PTSD rats than in the normal control group. Conclusion SPS stimulation activated the signal transduction pathway of p38-CHOP, leading to the apoptosis of dorsal raphe nucleus.