Yaxuan Wang1, Xuezhao Cao2, Hong Ma3, Wenfei Tan4, Lingwei Zhang5, Zhe Li6, Yalei Gao7. 1. Department of Anesthesiology, the first Affiliated Hospital of China Medical University, Nanjing North Street 155, Shenyang, Liaoning, China. Electronic address: yaxuanwangcmu@126.com. 2. Department of Anesthesiology, the first Affiliated Hospital of China Medical University, Nanjing North Street 155, Shenyang, Liaoning, China. Electronic address: xuezhaocao2011@hotmail.com. 3. Department of Anesthesiology, the first Affiliated Hospital of China Medical University, Nanjing North Street 155, Shenyang, Liaoning, China. Electronic address: mahong5466@yahoo.com. 4. Department of Anesthesiology, the first Affiliated Hospital of China Medical University, Nanjing North Street 155, Shenyang, Liaoning, China. Electronic address: winfieldtan@hotmail.com. 5. Department of Anesthesiology, the first Affiliated Hospital of China Medical University, Nanjing North Street 155, Shenyang, Liaoning, China. Electronic address: weilingwei1989@126.com. 6. Department of Anesthesiology, the first Affiliated Hospital of China Medical University, Nanjing North Street 155, Shenyang, Liaoning, China. Electronic address: jllizhe@126.com. 7. Department of Anesthesiology, the first Affiliated Hospital of China Medical University, Nanjing North Street 155, Shenyang, Liaoning, China. Electronic address: yaleigao@163.com.
Abstract
UNLABELLED: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
UNLABELLED: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
Authors: Na Wang; Hong Ma; Zhe Li; Yalei Gao; Xuezhao Cao; Yanhua Jiang; Yongjian Zhou; Sidan Liu Journal: PLoS One Date: 2017-08-14 Impact factor: 3.240
Authors: Andrea Comella Bolla; Tony Valente; Andres Miguez; Veronica Brito; Silvia Gines; Carme Solà; Marco Straccia; Josep M Canals Journal: PLoS One Date: 2019-12-02 Impact factor: 3.240