褪黑素对新生鼠缺氧缺血性脑损伤表达NF-κB的影响  

Effects of melatonin on NF-κB expression in hypoxia ischemia brain damage in neonatal rats

作　　者：顾镜月[1] 安亮[1] 梅梅[1] 杨松[1] 

机构地区：[1]佳木斯大学附属第一医院儿一科,黑龙江佳木斯154003

出　　处：《黑龙江医药科学》2012年第1期37-38,共2页Heilongjiang Medicine and Pharmacy

摘　　要：目的:探讨褪黑素(melatonin,MT)对新生大鼠缺氧缺血性脑损伤的神经保护作用及作用机制。方法:新生健康7日龄Wistar大鼠120只,随机分为3组:假手术组(40只)、缺氧缺血模型组(40只)、MT治疗组(40只),参照经典方法建立新生大鼠缺氧缺血性脑损伤(HIBD)模型,MT治疗组于模型制作完成后立刻注射MT10mg/kg1次于腹腔内,脑损伤组则于腹腔内注射等量的0.9%氯化钠注射液。各组分别于手术后6、24、48、72 h取脑组织切片,免疫组织化学方法检测核因子-κB(NF-κB)的表达.结果:与假手术组相比,缺氧缺血组NF-κB表达随时间的变化增加显著(P<0.01)。与缺氧缺血组相比较,MT治疗组NF-κB表达在12,24,48h三个时间点中下降显著(P<0.01)。结论:MT对HIBD后海马区神经细胞具有保护作用,其作用机制可能与抑制NF-κB在海马区的持续活化有关。Objective：To investigate the effect of melatonin on neonatal rat hypoxic-ischemic brain injury and nerve protection mechanism.Methods：One hundred and twenty 7-days-old wistar rats were randomly divided into 3 groups： control group（n=40）,hypoxia-ischemic group（n=40） and MT-treated group（n=40）.The hypoxia-ischemic brain damage（HIBD） model was established via Rice method.The rats in MT-treated group received a single dose of MT10mg/kg intra-peritoneally after hypoxia-ischemic brain injury and the rats in HIBD group received equal amount of normal saline intra-peritoneally.The brain tissue of rats in all experimental groups were harvested at 6,24,48 and 72h after surgery and the NF-κB expression in the hippocampus was measured by immunohistochemical technique.Results：Compared with control group,the level of NF-κB expression was increased significantly with duration of hypoxia-ischemic brain injury of rats in HIBD group（P0.01）.Compared with hypoxia-ischemic group and the level of NF-κB expression in MT-treated group was decreased significantly at 24,48 and 72h（P0.01）.Conclusion：The protective mechanism of MT may be related to the inhibition of persistent activation of NF-κB.

关 键 词：褪黑素 缺氧缺血 脑 信号传导 核因子-ΚB 

分 类 号：R743[医药卫生—神经病学与精神病学]