Aβ1-40脑内注射对大鼠海马超氧化物歧化酶丙二醛影响及通络救.docVIP

Aβ1-40脑内注射对大鼠海马超氧化物歧化酶丙二醛影响及通络救 　 作者：张晓杰，张春庆，胡南，宫国良，李澎涛 【摘要】 目的观察通络救脑口服液对β-淀粉样蛋白1 - 40 (Aβ1-40 )诱导的AD模型大鼠海马SOD活性和MDA蛋白表达的影响。方法选用140只SD雄性大鼠随机分为空白对照组、假手术组、模型组、盐酸多奈哌齐组、通络救脑口服液各剂量组(12，24，48 mg·kg-1·d-1)共7组，每组20只。采用海马立体定向注射凝聚态Aβ1 - 40建立老年性痴呆(Alzheimer’s disease， AD)动物模型。药物干预4周，第5周应用分光光度法检测大鼠大脑海马组织SOD、MDA蛋白的表达。结果与空白对照组比较，模型组SOD活性明显降低(Plt;0.05)，而MDA含量明显升高(Plt;0.05);与模型组比较，盐酸多萘哌齐组、通络救脑口服液各剂量组SOD活性明显升高(Plt;0.05)，而MDA含量明显降低(Plt;0.05)。结论通络救脑口服液通过上调SOD的活性和抑制MDA的表达而发挥其抗氧化治疗老年性痴呆的作用。 【关键词】 阿尔茨海默氏病; 通络救脑口服液; 超氧化物歧化酶; 丙二醛 　　Abstract：ObjectiveTo observe the effect of TLJN Oral Solution on protein SOD, MDA expression in brain tissue of amyloid-β1-40 injection into Hippocampus-induced experimental AD rats in vivo. Methods140 SD rats were enrolled in the study, and they were equally randomly divided into blank control group,sham control group, negative control group, positive control group and experiment group(12,24,48 mg·kg-1·d-1).A rat model of AD was induced by amyloid-β1-40 sterotaxis injection into the bilateral hippocaupa. All rats were sacrificed in the 5th week after treatment for 4 weeks. The total activity of SOD and level of MDA in brain tissue were detected by ultraviolet-spectrophotometry.ResultsThe SOD activity was decreased in model groups (Plt;0.05)compared with the sham group and MDA level was increased. In experiment groups the SOD activity was increased and MDA content was reduced compared with the model group (Plt;0.05).ConclusionTLJN Oral Solution can up-regulate expression of SOD and down-regulate expression of MDA. TLJN Oral Solution can inhibit the incidents of Alzheimer’s disease by antioxidative effect. 　　Key words：Alzheimer’s disease; TLJN Oral Solution; SOD; MDA 　　老年性痴呆(Alzheimer’s disease ,AD)又称阿尔茨海默病, 是一种以进行性认知障碍和记忆能力损害为主的中枢神经系统退行性疾病。其特征性病理变化是患者脑内的神经炎性斑，它是细胞外β-淀粉样蛋白(β-amyloid,Aβ)沉积而形成的[1]。阿尔茨海默病是一类多病因疾病，研究表明，自由基损伤和氧化应激是导致阿尔茨海默病大脑神经元损伤的重要原因[2]，血清超氧化物歧化酶(superoxide dismutase, SOD)和丙二醛(malon-dialdehyde,MDA) 与阿尔茨海默病的发生发展有密切的关系[3]。本实验采用大脑海马立体定向注射