JAK2/STAT3通路参与大鼠坐骨神经结扎神经病理性疼痛模型

JAK2 / STAT3 pathway is involved in bilateral chronic constriction injury rat neuropathic pain model

目的结扎大鼠双侧坐骨神经复制bCCI模型,观察JAK2/STAT3通路的激活情况。方法 60只体质量180~200 g SD雌性大鼠随机分为3组,bCCI组,sham组及Nave组。分别于bCCI手术术前1 d,术后3、7、14和21d取腰段脊髓背角,并进行RT-PCR及Western blot观察通路中主要因子的mRNA水平及蛋白水平的变化。结果 bCCI组大鼠对机械、热刺激及冷丙酮刺激的痛觉阈值明显降低。与sham组及Nave相比,bCCI组STAT3、SOCS3、JAK2及IL-6 mRNA水平显著升高,且3组在不同时间点具有差异（P〈0.05）。与sham组及Nave相比,bCCI组P-STAT3、JAK2和SOCS3蛋白水平升高。结论大鼠bCCI神经病理性疼痛模型JAK2/STAT3通路激活。

Objective To evaluate the contribution of the JAK2 / STAT3 pathway to neuropathic pain by animal model. Methods A rat model of bCCI was established and 60 rats＇ behavior tests were performed on the day before surgery and on day 3,7,4 and 21 after surgery,L4 ~ L6 dorsal spinal cord was harvested at the each time point. RT-PCR and Western blot were performed to explore the activation of JAK2 / STAT3 pathway. Results Pain-related behavioral tests socres in the bCCI rats were significant decreased as compared to the sham-operated and nave group at each time point postoperatively（ P 〈0. 05）. SOCS3 mRNA and STAT3 mRNA significantly increased on day 14,accompanied by JAK2 mRNA of with a similar time course. IL-6 mRNA level increased on day 3 and showed statistically significant increases on day 21. Western blot analysis showed that JAK2,P-STAT3,SOCS3 in-creased at different timepoints. Conclusion Our results suggest that the JAK2 / STAT3 pathway in the spinal dorsal horn was significantly upregulated in a rat bCCI model of neuropathic pain which will open new avenues for thera-peutic intervention.