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目的:观察补肾化痰法对AD模型大鼠CaMKⅡ-α活性的影响并探讨其可能机制。方法:应用脑立体定向技术给大鼠BNM注射凝聚态Aβ25-35+IBO构建AD模型。注射2周后,高、中、低量组分别给大鼠该药水煎液灌胃;西药组用哈伯因混悬液灌胃;正常组、空白组、模型组均给予等容积的生理盐水灌胃。28d后采用原位杂交法检测海马神经元CaMKⅡ-α水平的变化。结果在正常大鼠的脑海马部位少见CaMKⅡ-α免疫阳性表达,正常组与空白组无明显差异(P>0.05),而在模型组可见大量的棕黄色CaMKⅡ-α免疫阳性表达,与正常组相比,具有统计学差异(P<0.01)。西药组与模型组比较无差异(P>0.05),中药中高量组阳性表达较模型组均有所减少(P<0.01)。低量组与模型组无差异(P>0.05),但与西药组有一定差异(P<0.05)。结论:补肾化痰法可以可能通过抑制CaMKⅡ-α的活性,降低Tau蛋白异常磷酸化水平,从而发挥其抗老年性痴呆的作用
Objective: To observe the effect of Tonifying Kidney and Eliminating Phlegm Method on CaMKⅡ-α activity in AD model rats and to explore its possible mechanism. Methods: AD model was established by injection of condensed Aβ25-35 + IBO into rat BNM by stereotactic technique. After 2 weeks of injection, rats in the high, medium and low dose groups were orally administered with the decoction of the medicinal solution respectively; the western medicine group was administered with a suspension of Habituin; the normal group, the blank group and the model group were given equal volumes of normal saline Gavage. After 28 days, the level of CaMKⅡ-α in hippocampal neurons was detected by in situ hybridization. Results There was no expression of CaMKⅡ-α in normal hippocampus of normal rats. There was no significant difference between normal group and blank group (P> 0.05), but a large amount of brown CaMKⅡ-α immunoreactivity was found in model group, Compared with statistically significant (P <0.01). Western medicine group and the model group no significant difference (P> 0.05), medium and high levels of Chinese medicine group compared with the model group, the positive expression decreased (P <0.01). There was no difference between the low dose group and the model group (P> 0.05), but there was a certain difference between the low dose group and the western medicine group (P <0.05). Conclusion: Bushenhuatan method may play an anti-senile dementia effect by inhibiting the activity of CaMKⅡ-α, reducing the abnormal phosphorylation of Tau protein