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作 者:朱婧 李鑫 朱利娟 康涛[2] 高娜[3] ZHU Jing;LI Xin;ZHU Li-juan;KANG Tao;GAO Na(Department of Anesthesiology,Shaanxi Provincial People's Hospital,Xi'an,Shaanxi,710068,China;Department of Neurology,Shaanxi Provincial People's Hospital,Xi'an,Shaanxi,710068,China;Department of Pediatrics,Shaanxi Provincial People's Hospital,Xi'an,Shaanxi,710068,China)
机构地区:[1]陕西省人民医院麻醉科,陕西西安710068 [2]陕西省人民医院神经内科,陕西西安710068 [3]陕西省人民医院儿科,陕西西安710068
出 处:《现代生物医学进展》2021年第24期4637-4640,4622,共5页Progress in Modern Biomedicine
基 金:陕西省自然科学基础研究计划(2018JM7121)。
摘 要:目的:探讨不同剂量苯巴比妥钠对缺血性脑损伤大鼠神经功能及认知障碍恢复的影响。方法:将缺血性脑损伤大鼠(n=48)随机平分为三组-模型组、低剂量组与高剂量组。造模后第7 d起,模型组、低剂量组与高剂量组分别给予腹腔注射生理盐水、苯巴比妥钠50 mg/kg/d与苯巴比妥钠100 mg/kg/d,持续7 d,观察与记录大鼠神经功能及认知障碍恢复情况。结果:低剂量组与高剂量组治疗第3 d与第7 d的寻台潜伏期与跨越原平台位置时间都少于模型组(P<0.05),血清丙二醛(malondialdehyde,MDA)含量低于对照组(P<0.05),超氧化物歧化酶(Superoxide dismutase,SOD)活性高于模型组(P<0.05),低剂量组与高剂量组对比差异无统计学意义(P>0.05)。低剂量组与高剂量组治疗第7 d的脑组织细胞指数高于模型组(P<0.05),Bcl-2、NF-κB p65蛋白相对表达水平低于模型组(P<0.05),低剂量组与高剂量组对比差异无统计学意义(P>0.05)。结论:低剂量苯巴比妥钠在缺血性脑损伤大鼠的应用就能抑制Bcl-2、NF-κB p65蛋白的表达,也可抑制脑组织细胞凋亡,能促进SOD的释放与降低MDA的含量,有利于促进大鼠学习记忆与工作记忆能力的恢复。Objective:To investigate the effects of different doses of phenobarbital sodium on the recovery of neurological function and cognitive impairment in rats with ischemic brain injury.Methods:The rats with ischemic brain injury(n=48)were randomly equally divided into three groups-model group,low-dose group and high-dose group.From the 7 th day after modeling,the model group,low-dose group and high-dose group were given intraperitoneal injection of normal saline,phenobarbital sodium 50 mg/kg/d and phenobarbital sodium 100 mg/kg/d,for 7 days,observed and recorded the recovery of neurological function and cognitive impairment in rats.Results:The platform seeking latency and time to cross the original platform in the low-dose group and the high-dose group on the 3 rd and 7 th day of treatment were less than the model group(P<0.05),and the serum malondialdehyde(MDA)content were lower than that of the control group(P<0.05),the activity of superoxide dismutase(SOD)were higher than that of the model group(P<0.05),and there were no significant difference compared between the low-dose group and the high-dose group(P>0.05).The brain tissue cell index of the low-dose group and the high-dose group on the 7 th day of treatment were higher than that of the model group(P<0.05),the relative expression levels of Bcl-2 and NF-κB p65 protein were lower than the model group(P<0.05),and there were no significant difference compared between the low-dose group and the high-dose group(P>0.05).Conclusion:The application of low-dose phenobarbital sodium in rats with ischemic brain injury can inhibit the expression of Bcl-2,NF-κB p65 protein,can also inhibit cell apoptosis in brain tissue,and can promote the release and decrease of SOD The content of MDA,so it is beneficial to promote the recovery of learning memory and working memory in rats.
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