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首页> 外文期刊>Journal of Medical Sciences >Neuroprotective Effect of Post Ischemic Treatment of Acetylsalicylic Acid on CA1 Hippocampus Neuron and Spatial Learning in Transient MCA Occlusion in Rat
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Neuroprotective Effect of Post Ischemic Treatment of Acetylsalicylic Acid on CA1 Hippocampus Neuron and Spatial Learning in Transient MCA Occlusion in Rat

机译：乙酰水杨酸缺血后处理对大鼠短暂性MCA闭塞对CA1海马神经元和空间学习的神经保护作用

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The present study was designed to examine the neuroprotective effects of post-ischemic treatment with ASA on pyramidal neurons of the hippocampal CA1 sector and spatial learning and memory. Animals were allocated to ASA (20, 40 and 80 mg kg-1) and vehicle groups. Ischemia was induced by 20 min middle cerebral artery occlusion. ASA solution was administered intraperitoneal at 30 min, 6 and 24 h after induction of ischemia. Four days after ischemia, animals were subjected to 5 days of training in the Morris water maze (MWM); 4 days with the invisible platform to test spatial learning and the 5th day without platform to test spatial memory. At the end of behavioral test rats were sacrificed and pyramidal neurons in the CA1 sector were stained with Hematoxylin and Eosin. We demonstrated that repeated injections of 20 mg kg-1 ASA (p-1 ASA (p = 0.989) increased percentage of spent time in the target zone across the four days post stroke test period significantly in the MWM as compared to vehicle group. But repeated injections of 20, 40 and 80 mg kg-1 of ASA after ischemia not reduced the prolongation of the escape latency significantly as compared to vehicle group (p = 0.556). In treated groups there was no significant effect on spatial memory (p = 0.987) as compared to vehicle group. Histological verification of CA1 area showed that repeated injections of 20, 40 and 80 mg kg-1 ASA at 30 min, 6 and 24 h after ischemia reduced the number of dead hippocampal neuronal cells significantly (p<0.001). Study findings show that repeated ASA injections at 30 min, 6 and 24 h after stroke onset decreases neuronal injuries following ischemia and attenuates cerebral ischemia-induced learning dysfunctions.
机译：本研究旨在检查ASA缺血后治疗对海马CA1区锥体神经元和空间学习与记忆的神经保护作用。将动物分为ASA（20、40和80 mg kg -1 ）和媒介物组。缺血是由20分钟的大脑中动脉闭塞引起的。在诱导缺血后30分钟，6和24小时腹膜内施用ASA溶液。缺血四天后，在莫里斯水迷宫（MWM）中对动物进行5天训练。第4天使用隐形平台测试空间学习，第5天不用平台测试空间记忆。在行为测试结束时，处死大鼠，并用苏木精和曙红对CA1区的锥体神经元染色。我们证明，在中风测试期后的四天内，重复注射20 mg kg -1 ASA（p-1 ASA（p = 0.989），可以增加目标区域的花费时间百分比与溶媒组相比，MWM显着增加。但是与溶媒组相比，缺血后反复注射20、40和80 mg kg -1 ASA并没有显着延长逃逸潜伏期。 = 0.556）。与媒介物相比，治疗组对空间记忆没有显着影响（p = 0.987）。CA1区域的组织学验证显示，重复注射20、40和80 mg kg -1 ASA在缺血后30分钟，6和24小时显着减少了死亡海马神经元细胞的数量（p <0.001）。研究结果表明，在卒中发作后30分钟，6和24小时重复注射ASA可以减少神经元损伤缺血并减轻脑缺血引起的学习功能障碍。

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