丹参酮IIA对血管性痴呆小鼠的神经保护作用机制初探论文.docVIP

　　丹参酮IIA对血管性痴呆小鼠的神经保护作用机制初探论文 【摘要】 目的初步探讨丹参酮主要成分丹参酮IIA对血管性痴呆小鼠的神经保护作用机制。方法双侧颈总动脉反复缺血/再灌注合并尾部放血降压方法建立血管性痴呆小鼠模型。动物随机分为假手术组、缺血模型组、丹参酮IIA低、高剂量（4 mg/kg.d，8 mg/kg.d ）治疗组。手术20 d后开始运用Morris水迷宫观测各组的学习记忆功能，然后断头取脑，分离皮层和海马组织，分光光度法测定丙二醛(malondialdehyde, MDA) 含量和超氧化物歧化酶(superoxide dismutase, SOD)以及谷胱甘肽过氧化物酶（GSH-Px）活性的变化；运用高效液相色谱法测定不同组小鼠皮层和海马组织内谷氨酸和γ-氨基丁酸的含量。结果①丹参酮IIA可以改善血管性痴呆小鼠的学习记忆功能； ②丹参酮IIA可减少MDA的生成, 增加SOD、GSH-Px活性; ③小鼠手术20 d后，小鼠皮层和海马组织谷氨酸和γ-氨基丁酸的含量减低，丹参酮IIA可增加血管性痴呆小鼠皮层和海马组织内谷氨酸和γ-氨基丁酸的含量。结论丹参酮IIA在血管性痴呆小鼠可发挥抗氧化作用并调节兴奋性氨基酸和抑制性氨基酸的含量。 【关键词】 丹参酮IIA; 谷氨酸; γ-氨基丁酸； 血管性痴呆 Abstract：ObjectiveTo investigate the underlying neuroprotective mechanisms of Tanshinone IIA (TSA) on mouse cerebral ischemia in vivo.MethodsMale mice -operated, ischemic and treated groups (loice ia-reperfusion three times on bilateral mon carotid arteries by knots to establish models of vascular dementia. After ischemia-reperfusion impairment, TSA (4 mg/kg.d, 8 mg/kg.d) inistered by i.p. for 20 days in treated group. 1. DA), activity of superoxide dismetase (SOD) and glutathione peroxidase (GPX) in brain tissue eter; 3. High-performance liquid chromatography(HPLC) easure the contents of glutamate and gamma-aminobutyric acid (GABA) in cortex and hippocampus.Results①TSA can improve learning and memory deficits in vascular dementia; ②An elevation of SOD and GPX activity and decrease of MDA level ia; ③Decreased glutamate and gamma-aminobutyric acid induced by chronic brain ischemia arkedly inhibited by TSA pretreatment. ConclusionThe neuroprotective effect of TSA are partly due to its functions as folloate and gamma-aminobutyric acid. Key ate; GABA; Vascular dementia 血管性痴呆(vascular dementia,VD)是指由各种脑血管疾病引起的脑功能障碍而产生的获得性智能损害综合征,为一种慢性进行性疾病,其病理改变主要是以广泛性脑动脉硬化和脑梗塞为特征, 随着当今世界人口老龄化日益严重,其发病率日趋增高［1］。我国中药资源丰富,.freela 公司(St. Louis, MO, USA); β-巯基乙醇购自 AMRESCO Inc. (Ohio, USA); 邻苯二甲醛(O-phthaldialdehyde, OPA) 购自Sigma (St. Louis, MO, USA); 甲醇(色谱纯)购自Fisher Scientific (USA); 磷酸二氢钠、磷酸氢二钠、硼酸钠均为国产分析纯，实验前用四蒸水配成所需浓度；MDA, SOD,GSH-Px以及蛋