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远志总皂苷对阿尔茨海默病模型大鼠海马脑源性神经营养因子及酪氨酸蛋白激酶B表达的影响
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远志总皂苷对阿尔茨海默病模型大鼠海马脑源性神经营养因子及酪氨酸蛋白激酶B表达的影响
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远志总皂苷对阿尔茨海默病模型大鼠海马脑源性神经营养因子及酪氨酸蛋白激酶B表达的影响
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Journal Article
远志总皂苷对阿尔茨海默病模型大鼠海马脑源性神经营养因子及酪氨酸蛋白激酶B表达的影响
2014
Overview
目的观察远志总皂苷对阿尔茨海默病模型大鼠海马CA1区脑源性神经营养因子（BDNF）及其特异性受体酪氨酸蛋白激酶B（TrkB）表达的影响，探讨远志总皂苷对阿尔茨海默病的干预作用机制。方法雄性Wistar大鼠被随机分为生理盐水组（正常对照组）、阿尔茨海默病模型组（模型组），以及远志总皂苷低剂量（12．50mg／ml）和高剂量（37．50mg／ml）组；采用D-半乳糖致衰老联合鹅膏覃氨酸损毁基底前脑Meynert核法建立阿尔茨海默病大鼠模型，免疫组织化学染色检测大鼠海马CA1区BDNF及其受体TrkB表达水平。结果BDNF和TrkB阳性物质呈棕黄色，主要表达于海马CA1区神经元胞膜。模型组大鼠海马CA1区BDNF及其受体TrkB表达水平为0．30±0．02和0．21±0．07，低于正常对照组的0．47±0．02和0．46±0．05（均P=0．000）；与模型组相比，远志总皂苷低剂量组（0．35±0．05，0．32±0．07）和高剂量组（0．43±0．05，0．37±0．03）大鼠海马CA1区BDNF及其受体TrkB表达水平均显著升高（均P=0．000），但以高剂量组升高更为显著（均P=0．000）。结论远志总皂苷可以显著升高阿尔茨海默病模型大鼠海马CA1区BDNF及其受体TrkB表达水平，且具有剂量依赖性，这可能是其改善认知功能的机制之一。
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