摘要
目的探讨大鼠大脑海马注射β-淀粉样蛋白1--40对MA0、脂褐素表达的影响及通络救脑口服液对其的干预作用。方法140只Sprague--Dawley（SD）大鼠随机分为空白对照组、假手术组、阴性对照组、阳性对照组、实验组（48，24，12mg·kg^-1·d^-1）共7组。采用大脑海马立体定向注射凝聚态β-淀粉样蛋白14。诱导老年性痴呆（Alzheimer’Sdisease，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组织MA0酶活性的变化，采用荧光分光光度法检测脂褐素的含量变化，以及通络救脑口服液对上述指标的影响。结果模型组大鼠脑组织MA0、脂褐素含量分别为（7．88±0．76）和（5．42士0．24），MAO、脂褐素含量显著多于假手术组MA0含量为（5．38±0．52），脂褐素含量为（4．16±0．18），P〈0．05），表明模型组MA0、脂褐素表达水平升高；与模型组比较，盐酸多奈哌齐组MA0含量为（7．08±0．39），脂褐素含量为（4．91±0．23）、通络救脑口服液低、中、高各剂量组MAO分别为（7．07±0．81，7．13士0．53，6．36±0．36）；脂褐素分别为（4．89±0．17，4．52士0．20，4．23±0．35），MAO与脂褐素含量显著减少。结论大脑海马注射β-淀粉样蛋白1-40后大鼠脑组织MAO、脂褐素表达水平明显增高，而通络救脑口服液可以降低海马组织MA0、脂褐素的含量，通过其抗氧化而发挥其抗老年性痴呆的作用。
Objective To explore the effect of TLJN Oral Solution on the expression of monoamine oxidase （MAO） and Lipofuscin in brain tissue of rats with amyloid-β1--40 induced experimental Alzheimer＇s disease （AD） in vivo. Methods 140 SD rats enrolled in the study were randomly divided into blank control, sham control, negative control, positive control and experiment groups in which experiment group was further divided into three groups based on dose （12 mg · kg^-1·d^-1 , 24 mg · kg^-1·d^-1 , 48 mg · kg^-1·d^-1 ）. The model of AD was induced by injection of amyloid--β1--40 sterotaxis into rat bilateral Hippocampus. All rats were sacrificed in 5th week after 4--week treatment. The total activity of MAO in the brain tissue was determined by ultraviolet--spectrophotometry, and the content of lipofuscin was measured by spectrofluorimetry. Results The protein levels of Mao and Lipofuscin were up--regulated in the positive control group with 2--AACt values of 7. 88±0.76 and 5.42± 0.24 respectively, compared to the sham group （5. 38±0.52 and 4. 16±0.18, P〈0.05）. In experiment group, the protein levels of MAO and lipofuscin, however, were dramatically reduced with 2--AACt values of 7.07 ±0.81, 7. 13±0.53, 6. 36±0.36 and 4. 89±0. 17, 4. 52±0.20, 4. 23±0.35, respectively, compared to the positive control group. Conclusions The protein levels of MAO and lipofuscin were significantly elevated in brain tissue of rats with amyloid-β1- 40 induced experimental Alzheimer＇s disease, and that could be inhibited by TLJN Oral Solution, indicating that the TLJN Oral Solution may function as an antioxidant in the treatment and prevention of Alzheimer＇s disease.
出处
《神经疾病与精神卫生》
2009年第3期234-237,共4页
Journal of Neuroscience and Mental Health
基金
基金项目：齐齐哈尔市科学技术局资助项目（编号：SF-0805）
关键词
抗氧化
阿尔茨海默病
通络救脑口服液
分光光度法
MAO
脂褐素
Antioxidative
Alzheimer＇s disease
TLJN Oral Solution
Monoamine oxidase
Lipofusein
Ultraviolet--spectrophotometry
