神经病理性疼痛大鼠海马促炎性 细胞因子的表达水平变化

目的 观察腰5脊神经横断(L5-SNT)所致的神经病理性疼痛大鼠模型海马TNF-α、IL-1β、IL-6的不同时程表达水平变化。方法 将36只雄性SD大鼠随机分成3组:正常组(Z组)、假手术组(J组)和模型组(M组),每组各12只; 术后观察大鼠行为学变化并测量各组大鼠术前1 d及术后1～15 d机械缩足痛阈值(MWT); 选择术后不同时间点2、7、11、15 d随机取大鼠(3只/时间点/组),应用RT-PCR法检测海马TNF-α、IL-1β及IL-6的表达水平。结果 ①与术前1 d比较,M组大鼠术后手术侧MWT迅速降低(P<0.01),与Z组及J组比较,M组大鼠手术侧50% MWT明显下降(P<0.01); ②与J组比较,M组大鼠海马TNF-α于术后第2 d开始增高,第7 d达高峰,并且直到术后11 d仍保持较高水平(P<0.05); IL-1β在术后第11 d表达水平明显上调(P<0.05); IL-6在术后第2 d表达水平增高(P<0.05),并且在术后第7、11及15 d仍处于较高水平。结论 SNT导致大鼠海马TNF-α、IL-1β、IL-6表达水平上调,其机制可能与海马参与神经病理性疼痛的调控密切相关。

Expression level change of proinflammatory cytokines in the hippocampus of rats with neuropathic pain

ObjectiveTo observe the expression level changes of TNF-α, IL-1β and IL-6 in the hippocampus of rats suffered from neuropathic pain, which were induced by L5 spinal nerve transection(L5-SNT).Methods Thirty-six male Sprague-Dawley rats were randomly divided into three groups: normal group(Z group )(n=12), sham operation group(J group)(n=12)and model group(M group)(n=12). The behavior changes of rats were observed after operation, and the mechanical withdrawl threshold(MWT)were measured at 1d before operation and 1～15 d after operation. The rats were randomly selected at 2, 7, 11and 15 d(3/time point/ group). The expression levels of TNF-α, IL-1β and IL-6 in hippocampus were detected by RT-PCR.Results ① Compared with the 1 d before operation, the mechanical pain threshold of M group was decreased rapidly(P<0.01). Compared with Z group and J group, the 50% MWT of M group was significantly decreased(P<0.01). ② RT-PCR revealed that TNF-α expression level in hippocampus of M group began to increase at 2 d after operation, reached peak at 7 d and still maintained at a high level at 11 d after operation(P<0.05); IL-1β expression level increased on the 11 d after operation(P<0.05). The expression level of IL-6 increased on the 2 d after operation(P<0.05), and still maintained at a high level at 7, 11 and 15 d after operation.Conclusion SNT could up-regulate the expression levels of TNF-α, IL-1β and IL-6 in hippocampus of rats, which might be closely related to the regulation of hippocampus involvement in neuropathic pain.