Wang Yaxuan, Cao Xuezhao, Ma Hong, Tan Wenfei, Zhang Lingwei, Li Zhe, Gao Yalei
Department of Anesthesiology, the first Affiliated Hospital of China Medical University, Nanjing North Street 155, Shenyang, Liaoning, China.
Brain Res. 2016 Oct 1;1648(Pt A):380-386. doi: 10.1016/j.brainres.2016.07.045. Epub 2016 Jul 31.
Increasing evidence indicates that stress potentiates pro-inflammatory response to a subsequent peripheral immune challenge. The present study investigated if prior exposure to inescapable tailshock (IS) delayed the recovery of surgery-induced spatial learning and memory impairment and prolonged hippocampus interleukin (IL)-1β and IL-6 expression.
A total of 192 aged rats were trained with Morris water-maze (MWM) for 6 consecutive days. A single session of inescapable tailshock was performed on day 6 after training. Then, the rats subjected to partial hepatectomy. Hippocampal-dependent spatial learning and memory were assessed on postoperative days 1, 3 and 7. The cytokines IL-1β and IL-6 and ionized calcium binding adaptor protein (Iba)-1 were measured at each time point. Cluster of differentiation 200 (CD200) was also measured to explore potential mechanisms of glial cell activation.
Exposure of IS alone failed to affect the latency to platform and increase hippocampal cytokine levels at each time point. However, IS alone significantly increased the expression levels of Iba-1. A prolonged latency and additional significant increase in hippocampal levels of IL-1β and IL-6 were observed when partial hepatectomy was performed in aged rats exposed to IS 24h later. The combination of IS and surgical trauma dramatically upregulated the levels of Iba-1 and significantly decreased the expression of CD200.
IS alone failed to induce cognitive deficits and increase pro-inflammatory cytokines expression. However, IS delayed the recovery of surgery-induced spatial learning and memory impairment and prolonged pro-inflammatory response to the subsequent surgery challenge.
越来越多的证据表明，应激会增强对随后外周免疫挑战的促炎反应。本研究调查了先前暴露于不可逃避的尾部电击（IS）是否会延迟手术诱导的空间学习和记忆损伤的恢复，并延长海马白细胞介素（IL）-1β和IL-6的表达。
总共192只老年大鼠连续6天用莫里斯水迷宫（MWM）进行训练。在训练后的第6天进行单次不可逃避的尾部电击。然后，对大鼠进行部分肝切除术。在术后第1、3和7天评估海马依赖性空间学习和记忆。在每个时间点测量细胞因子IL-1β和IL-6以及离子钙结合衔接蛋白（Iba）-1。还测量了分化簇200（CD200）以探索胶质细胞激活的潜在机制。
单独暴露于IS未能影响到达平台的潜伏期，也未在每个时间点增加海马细胞因子水平。然而，单独的IS显著增加了Iba-1的表达水平。当在24小时后暴露于IS的老年大鼠中进行部分肝切除术时，观察到潜伏期延长以及海马IL-1β和IL-6水平进一步显著升高。IS与手术创伤的联合显著上调了Iba-1的水平，并显著降低了CD200的表达。
单独的IS未能诱导认知缺陷和增加促炎细胞因子表达。然而，IS延迟了手术诱导的空间学习和记忆损伤的恢复，并延长了对随后手术挑战的促炎反应。
