阿尔茨海默病模型大鼠血清beta-淀粉样蛋白的变化与补肾填精方的预防效应

Changes of Beta-amyloid Protein and Prevention Effect of Kidney-nourishing Decoction in Alzheimer's Disease Model Rats

目的 :研究血清 beta-淀粉样蛋白 ( beta- amyloid protein,Abeta)在阿尔茨海默病( Alzheimer’s disease,AD)模型大鼠中的变化及补肾填精方防治 AD大鼠的效应和机制。方法 :用腹腔注射 Al Cl3 ,复制大鼠 AD模型。用 Y电迷宫仪测定正常组、模型组和中药防治组大鼠的逃避正确率、逃避潜伏期和逃避行为方式。用放免法测定血清 Abeta含量。结果 :AD模型大鼠的血清Abeta水平显著升高 ,逃避行为方式异常 ,逃避潜伏期延长 ,逃避正确率降低 ,学习记忆能力明显损害。补肾填精方明显抑制 Al Cl3 引起的血清 Abeta的升高 ,纠正逃避行为方式异常 ,提高大鼠的逃避正确率 ,缩短逃避潜伏期 ,改善学习记忆能力。结论 :血清 Abeta水平变化主要由血小板功能的变化引起 ,血清 Abeta水平和脑损伤明显正相关 ,和学习记忆能力明显负相关。血清 Abeta水平升高可作为 AD诊断的血液指标。通过抑制免疫系统和血小板的过度激活 ,降低血清 Abeta含量 ,降低中枢神经系统的兴奋性 ,是补肾填精中药方防治铝致 AD大鼠学习记忆功能障碍的作用机制。

Objective: To study the changes of Beta amyloid protein and the preventive effects and mechanisms of kidney nourishing Decoction in Alzheimer's Disease (AD) model rats.Methods:Peritoneal injections of AlCl 3 were made to create the AD model rats and labyrinth device was used to detect the escaping rate, escaping latency and escaping behavior in normal, AD model and TCM groups. Radioimmunoassay was used to detect the Beta amyloid protein.Results: Beta amyroid protein in AD model group was raised with decreased escaping rate and increase escaping latency and abnormal escaping behaviors. Kidney nourishing Decoction could inhibit the amyroid protein expression induced by AlCl 3 with the corrected escaping behavior, increased escaping rate, decreased the escaping latency and improve the memory. Conclusion:Beta amyloid protein change was induced by platelet and positive correlated with cerebral damage and negatively correlated with study and memory, which could serve as an index for the diagnosis of AD. The mechanism lies on inhibiting the immune function and excessive platelet activation, lowering the serum amyloid protein and lowering the cerebral nervous system function with kidney nourishing decoction