Department of Anesthesiology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, China.
Curr Med Sci. 2018 Aug;38(4):666-671. doi: 10.1007/s11596-018-1928-8. Epub 2018 Aug 20.
The aim of the present study was to investigate the effect of lipoxin A4 (LXA4) pretreatment on cognitive function of aged rats after global cerebral ischemia reperfusion, and to explore its possible mechanism. Thirty-six aged male Sprague-Dawley rats were randomly divided into three groups (n=2 each): sham-operation group (S group), global cerebral ischemia reperfusion group (I/R group) and LXA4-pretreatment group (L group). The rat model of global cerebral ischemia reperfüsion was established by occlusion of the bilateral common carotid artery with hypotension. The cognitive function of rats was determined by a step-down type passive avoidance test and Morris Water Maze test on the third day after reperfUsion. Rats were sacrificed after Water Maze test and the pathological changes of hippocampal CAI region were observed and the related inflammatory mediators were determined. As compared with S group, the escape latency in I/R group was prolonged from the first day to the fifth day, while that in L group was prolonged from the first day to the third day. The retention time in I/R group and L group in the first quadrant was shortened. The reaction time, frequency of reaction mistake and frequency of escape mistake in I/R group increased, and the latent period shortened. The frequency of escape mistake in L group increased, and the damage in the hippocampal CAI region of I/R group and L group was obvious. The levels of S-100β, TNP-α, IL-lβ, IL-10 and NF-κB in I/R group and L group increased. As compared with I/R group, the escape latency in L group was shortened from the first day to the fifth day, and the retention time in the first quadrant prolonged. The reaction time, frequency of reaction mistake and frequency of escape mistake in L group decreased, and the latent period prolonged. The damage in the hippocampal CAI region of L group was alleviated as well. The levels of S-100β, TNP-α, IL-lβ and NF-κB in L group decreased, and those of IL-10 increased. It can be concluded that LXA4 pretreatment can improve the cognitive function in aged rats after global cerebral ischemia reperfusion probably by inhibiting the inflammatory reaction.
研究脂氧素 A4（LXA4）预处理对老龄大鼠全脑缺血再灌注后认知功能的影响，并探讨其可能的机制。
36 只雄性 Sprague-Dawley 老龄大鼠随机分为三组（每组 2 只）：假手术组（S 组）、全脑缺血再灌注组（I/R 组）和 LXA4 预处理组（L 组）。采用双侧颈总动脉夹闭低血压法建立全脑缺血再灌注模型。再灌注后第 3 天通过跳台型被动回避试验和 Morris 水迷宫试验测定大鼠的认知功能。水迷宫试验结束后处死大鼠，观察海马 CA1 区病理改变，测定相关炎症介质。
与 S 组比较，I/R 组大鼠自第 1 天至第 5 天逃避潜伏期延长，L 组自第 1 天至第 3 天逃避潜伏期延长；I/R 组和 L 组大鼠第 1 象限停留时间缩短，I/R 组大鼠反应时间延长，反应错误和逃避错误次数增加，潜伏期缩短；L 组大鼠逃避错误次数增加，海马 CA1 区损伤明显。I/R 组和 L 组大鼠 S-100β、肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）、白细胞介素-10（IL-10）和核因子-κB（NF-κB）水平升高。与 I/R 组比较，L 组大鼠自第 1 天至第 5 天逃避潜伏期缩短，第 1 象限停留时间延长，反应时间缩短，反应错误和逃避错误次数减少，潜伏期延长；L 组大鼠海马 CA1 区损伤减轻，S-100β、TNF-α、IL-1β和 NF-κB 水平降低，IL-10 水平升高。
LXA4 预处理可改善老龄大鼠全脑缺血再灌注后认知功能，其机制可能与抑制炎症反应有关。
