【摘 要】
：
目的 通过观察缺血性卒中后内源性抑郁大鼠额叶及杏仁核的脑源性生长因子(BDNF)、受体酪氨酸激酶B (TrkB)及磷酸化酪氨酸激酶B(pTrkB)的表达,探讨缺血性卒中后内源性抑郁的发病机制.方法 将SD雌性大鼠随机分为对照组、模型组和雌激素组.对照组去卵巢,不予任何刺激;模型组去卵巢1周后,予以大脑中动脉栓塞术(Middle cerebral artery occlusion,MCAO)后饲养2
【机 构】
：
温州医科大学附属第一医院神经内一科 325000
论文部分内容阅读
目的 通过观察缺血性卒中后内源性抑郁大鼠额叶及杏仁核的脑源性生长因子(BDNF)、受体酪氨酸激酶B (TrkB)及磷酸化酪氨酸激酶B(pTrkB)的表达,探讨缺血性卒中后内源性抑郁的发病机制.方法 将SD雌性大鼠随机分为对照组、模型组和雌激素组.对照组去卵巢,不予任何刺激;模型组去卵巢1周后,予以大脑中动脉栓塞术(Middle cerebral artery occlusion,MCAO)后饲养2周,再给予2周大豆油注射;雌激素组,去卵巢1周后,MCAO术后并饲养2周,再给予10μg溶于大豆油的0.1ml的雌激素干预2周.去卵巢1周后、饲养2周后和雌激素干预2周后分别予强迫游泳以观察行为学变化.使用免疫组化和蛋白质印迹的方法,观察BDNF和TrkB/pTrkB在额叶和杏仁核中的蛋白表达.
其他文献
目的 探讨反馈式功能性电刺激治疗对脑卒中后上肢运动功能恢复的影响及其fMRI机制.方法 21例脑卒中患者随机分为反馈式功能性电刺激组(实验1组)8人,功能性电刺激组(实验2组)7人,对照组6人,三组患者均进行常规神经内科药物治疗和康复治疗,实验1组进行反馈式功能性电刺激治疗,实验2组行功能性电刺激治疗,疗程4周.治疗前后行FugI-Meyer上肢评分,腕背伸角度,fMRI进行脑M1区激活强度检查.
目的 缺血性中风严重危害人类健康,随着对该病的临床观察与实践总结,逐渐形成了缺血性中风"毒损脑络"的病机假说.通络救脑注射液是针对缺血性脑卒中"毒损脑络"病机研发的现代注射剂.缺血激活的小胶质细胞不仅释放炎症因子促进神经元死亡,还分泌了神经保护性因子.平衡其所释放神经毒性因子跟神经保护因子的平衡是小胶质细胞功能稳定的关键,亦是药物作用调控的关卡.本研究以小胶质细胞为研究对象,对比该注射液及其两个有
Objective To investigate the neuroprotective mechanism of exogenous hydrogen sulfide on rats after cerebral ischemia-reperfusion by ERK-CREB pathway.Methods A total of 180 Sprague-Dawley male rats wer
目的 探讨NINJ2基因多态性与LAA型脑梗死的相关性,并初步探讨遗传因素对动脉粥样硬化血管床选择性损害的影响.方法 采用病例对照研究,选取286例LAA型脑梗死患者和298例同期非脑梗死人群,选取NINJ2基因4个代表性单核酸多态性[rs11833579 (G/A)、rs12425791 (G/A)、rs10849373 (G/A)和rs 11063806(G/A)],应用聚合酶链反应限制性片段
Oxidative damage plays a detrimental role in the pathophysiology of cerebral ischemia and may represent a therapeutic target.The transcription factor nuclear factor erythroid 2-related factor 2(Nrf2)
Stroke has a high incidence in the elderly.Stroke enters the chronic phase 3 months after initial stroke onset.Currently,there is no pharmaceutical treatment available for chronic stroke.We have demon
Inflammatory damage plays an important role in cerebral ischemic pathogenesis and represents a new target for treatment of stroke.Shikonin has gained attention for its prominent anti-inflammatory prop
Inflammatory damage plays an important role in cerebral ischemic pathogenesis and may represent a target for treatment.Parthenolide (PN) has been proved to elicit a wide range of biological activities
Gamma-secretase inhibitor,N-[N-(3,5-difluor-ophenacetyl)-1-alanyl]-S-phenylglycine t-butyl ester (DAPT) suppresses the activation of Notch 1 signaling,which is recognized as the cell fate signaling an
There is cumulative evidence that the serine-threonine kinase Akt and its downstream nuclear transcription factor CREB are involved in neuronal survival and protection.The Akt activates and phosphoryl