摘要
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。
Objective：To observe the effect of replenishing the kidney and eliminating phlegm therapy on calciumlcalmodulin-dependent protein kinase Ⅱ（CaMKⅡ-α） activities of AD rat model,and explore the potential mechanism.Methods：AD model was established by injection of ibotenic acid（IBO） and 25-35 β-amyloid peptide（Aβ25-35） into basal nucleus of Meynert.After injecting for two weeks,Bushen Huatan Decoction was administered by oral gavage of high,middle and low dosages.Huperzine A-Zhulin Antun tablets served as control drug.Normal group,model group and blank group were administered with isovolumetric saline water.After treating for four weeks,hybridization in situ was used to observe the change of CaMK Ⅱ in hippocamp.Results：The expression of CaMKⅡ-α in model group was more than that in normal group（P〈0.01）.Compared with model group,the expression of CaMKⅡ-α in middle and high dosages group decreased obviously（P〈0.01）.There was no obviouse difference between low dosage group and model group,but there was significant difference between low dosage group and Huperzine A-Zhulin Antun tablets group（P〈0.01）.Conclusion：Replenishing the kidney and eliminating phlegm therapy can inhibit AD by restraining the activity of CaMKⅡ-α and decreasing the level of tau protein hyper-phosphorylation.
出处
《中华中医药杂志》
CAS
CSCD
北大核心
2010年第5期786-788,共3页
China Journal of Traditional Chinese Medicine and Pharmacy
基金
国家中医药管理局基金项目(No.04-05JP41)
湖北省卫生厅科研基金项目(No.JX2B66)~~
关键词
补肾化痰法
ALZHEIMER
钙/钙调素依赖的蛋白激酶Ⅱ-α
TAU蛋白
Replenishing the kidney and eliminating phlegm therapy
Alzheimer
Calciurn/calmodulin-dependent protein kinaseII-α（CaMKII-α）
Tau protein
