甲状腺激素T3对大鼠脑缺血再灌注损伤后NGF和BDNF表达的影响研究  

The influence of thyroid hormones on the expression of NGF and BDNF after cerebral ischemia-reperfusion injury in rats

作　　者：窦超[1] 张敏[1] 赵源征[1] 郭亚培[1] 吴世陶[1] 刘恒方[1] 

机构地区：[1]郑州大学第五附属医院神经内科,郑州450000

出　　处：《重庆医学》2017年第15期2030-2033,共4页Chongqing medicine

基　　金：河南省医学科技攻关计划项目(16A310021)

摘　　要：目的探讨甲状腺激素T3对大鼠脑缺血再灌注损伤的神经保护作用及机制。方法雄性SD大鼠分为假手术+生理盐水组、假手术+T3组、大脑中动脉栓塞(MCAO)+生理盐水组、MCAO+T3组。应用MCAO法建立大鼠脑缺血再灌注损伤模型,分别于缺血后1h及再灌注后6h给予腹腔注射甲状腺激素10μg/100g,生理盐水为安慰剂。再灌注24h后,观察不同组别大鼠神经功能损伤情况,梗死体积变化,以及缺血侧脑皮质中神经生长因子(NGF)和脑源性神经营养因子(BDNF)的mRNA及蛋白表达水平变化。结果与MCAO+生理盐水组比较,MCAO+T3组大鼠神经功能缺损表现减轻,脑梗死体积减小,NGF、BDNF的mRNA和蛋白表达上升(P<0.05)。结论甲状腺激素对大鼠脑缺血再灌注损伤有神经保护作用,其机制与增加脑缺血再灌注损伤中NGF、BDNF的表达相关。Objective To investigate the neuroprotective effect of thyroid hormones T3 on cerebral ischemia-reperfusion injury in rats and its mechanism.Methods SD rats were divided into four groups：sham＋saline group,sham＋T3group,MCAO＋saline group,MCAO＋T3group.The cerebral ischemia-reperfusion injury rat models were established by right middle cerebral artery occlusion.Thyroid hormones（10μg/100g）or normal saline were given respectively by intraperitoneal injection twice at 1hafter the onset of ischemia and 6hafter reperfusion.Neurobehavioral score was evaluated at 24 hafter reperfusion;TTC staining was used to label infarction area;RT-PCR was used to detect the mRNA level of nerve growth factor（NGF）and brain derived neurotrophic factor（BDNF）in brain tissue;Western blot was employed to determine alterations in protein levels of NGF and BDNF.Results Compared with MCAO＋saline group,the neurological deficit and the volume of cerebral infarction of MCAO＋T3group was decreased,and the mRNA and protein expression of NGF and BDNF of MCAO＋T3group were increased（P〈0.05）.ConclusionThyroid Hormones could promote the nerve repair,stimulate the nerve regeneration and improve the nervous behavioral function by up-regulating the expression of NGF and BDNF.

关 键 词：脑缺血 再灌注损伤 甲状腺激素类 神经生长因子 神经保护作用 脑源性神经营养因子 

分 类 号：R743[医药卫生—神经病学与精神病学]