论文部分内容阅读
目的研究吴茱萸次碱(Rut)对脑缺血再灌注损伤小鼠学习记忆障碍的改善作用,探讨其可能的作用机制。方法昆明种♂小鼠50只随机分为假手术组、模型组、Rut各治疗组:Rut 84μg.kg-1组、Rut 252μg.kg-1组和Rut 504μg.kg-1组;采用阻断小鼠两侧颈总动脉5 min后再恢复血流制备小鼠脑缺血/再灌注模型,假手术组只穿线不缺血再灌注;Rut临用前用二甲基亚砜分别配置成所需浓度,于术前30 min腹腔注射给予Rut各治疗组,假手术组和模型组腹腔注射等量二甲基亚砜。脑缺血再灌注48 h后以避暗法考察小鼠的学习记忆能力,并测定小鼠脑组织中醛(MDA)含量、超氧化物歧化酶(SOD)的活力、谷胱甘肽过氧化物酶(GSH-Px)的活力。结果避暗实验中,与假手术组相比,模型组的潜伏期明显缩短,错误次数明显增加;与模型组相比,Rut各治疗组潜伏期显著延长,错误次数显著减少(P<0.01)。酶学实验中,与假手术组相比,模型组小鼠脑内MDA含量明显增加,SOD及GSH-Px活力显著降低(P<0.01);与模型组相比,Rut各治疗组小鼠脑内MDA含量明显减少,SOD及GSH-Px活力显著升高(P<0.01)。结论 吴茱萸次碱可以明显改善脑缺血再灌注损伤造成的小鼠学习记忆障碍,吴茱萸次碱通过提高小鼠脑内SOD及GSH-Px活力减少自由基的产生,减轻脑缺血再灌注造成的损伤。
Objective To study the effect of rututsk on the learning and memory impairment in mice with cerebral ischemia-reperfusion injury and to explore its possible mechanism. Methods Fifty Kunming mice were randomly divided into sham operation group, model group and Rut treatment group: Rut 84μg.kg-1 group, Rut 252μg.kg-1 group and Rut 504μg.kg-1 group. Mice in both sides of the common carotid artery 5min before resuming the flow of blood to prepare mouse model of cerebral ischemia / reperfusion, sham operation group only without ischemia and reperfusion perfusion; Rut before use with dimethyl sulfoxide were configured as The rats in Rut group were given intraperitoneal injection of 30 min preoperatively, and the rats in sham operation group and model group were intraperitoneally injected with dimethylsulfoxide (DMSO). Forty-eight hours after cerebral ischemia-reperfusion, the learning and memory abilities of mice were observed by dark-avoidance method. The contents of aldehyde (MDA), superoxide dismutase (SOD), glutathione peroxidation The enzyme activity (GSH-Px) activity. Results Compared with the sham group, the latency of the model group was significantly shortened and the number of errors significantly increased compared with the sham operation group. Compared with the model group, the latency of the Rut treatment group was significantly prolonged and the number of errors was significantly reduced (P <0.01). Compared with the sham group, the content of MDA in the model group increased significantly and the activities of SOD and GSH-Px decreased significantly (P <0.01). Compared with the model group, MDA content decreased significantly, SOD and GSH-Px activity increased significantly (P <0.01). Conclusions Rutaecarpine can significantly improve learning and memory deficits induced by cerebral ischemia-reperfusion injury in rats. Rutustrol can reduce the production of free radicals and increase the activity of SOD and GSH-Px in mice by relieving cerebral ischemia-reperfusion injury damage.