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作 者:毛青[1] 丁勇[1] 陆兆丰[2] 罗其中[2] 江基尧[2]
机构地区:[1]上海市浦东新区浦南医院神经外科 [2]上海交通大学附属仁济医院神经外科
出 处:《中华创伤杂志》2006年第10期758-762,共5页Chinese Journal of Trauma
摘 要:目的研究1-[2-(4-氯苯基)-2-羟基]乙基-4-[3,5-双(1,1-二甲基) -4-羟苯基]甲基哌嗪(AM-36)对颅脑外伤后继发性脑损害的神经保护作用。方法将38只SD大鼠随机分成研究组、对照组和假手术组后制作中度液压颅脑伤模型,致伤后30min、24h和48h分别给予研究组大鼠AM-36(0.1ml/100g)和后两组大鼠等量等渗盐水腹腔注射。致伤后24h行脑组织含水量测定,致伤后24h和1周对大鼠脑组织进行HE染色和Fluoro- Jade(F-J)染色,着重观察致伤部位周围皮层、丘脑及海马等区域的组织病理学改变。结果研究组大鼠伤后24h脑组织含水量较对照组明显减少,致伤后24h和1周,皮层、丘脑及海马CA1和CA3区的组织病理学检查显示研究组大鼠变性的F-J阳性神经元明显减少(P<0.05)。结论伤后早期系统应用AM-36能降低脑组织水含量,对大鼠液压颅脑伤有明显的神经保护作用。F-J染色能较准确地反映脑液压伤后的病理学改变,可用于组织病理学的定量分析。Objective To investigate neuroprotective effect of AM-36 on secondary brain injury following traumatic brain injury (TBI)in rats. Methods A total of 38 male Sprague-Dawley rats were divided into an experimental group, a control group and a sham operation group, then sustained to moderate TBI. AM-36 (0.1 ml/100 g) was administered intraperitoneally in the experimental group and isotonic saline solution was administered intraperitoneally in the control and the sham operation groups at 30 minutes, 24 and 48 hours after TBI, respectively. The brain water content was determined at 24 hours after TBI. Rats were sacrificed by decapitation at 24 hours or one week after TBI for observing histological changes in peripheral cortex, thalamus and hippocampus by means of Hematoxylin and Eosin staining and Fluoro-Jade (F-J) staining. Results The brain water content of bilateral hemispheres 24 hours after TBI in the experimental group was significantly decreased, compared to that of the control group. Histological examination revealed less degenerating neurons ( F-J positive neurons) in the cortex, thalamus, CA1 and CA3 of the hippocampus in AM-36 treated rats 24 hours and one week after injury(P 〈0.05). Conclusion Systemic administration of AM-36 at the early stage after TBI can decrease brain water content and exert neuroprotective effect on TBI. F-J staining can be used for histopathologic quantitation of neuronal damage, for it can accurately exhibit pathologic changes following TBI induced by fluid percussion.
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