中文摘要：

目的研究乌鸡白凤丸（BFP）对，β-淀粉样蛋白1-40（Aβ1-40）诱导体外培养大鼠海马神经元凋亡的保护作用以及可能的作用机制。方法体外培养新生Wistar大鼠海马神经元，MTT法检测不同浓度Aβ1-40m的细胞毒作用，选择出现显著细胞毒性的剂量为使用剂量。同时给予BFP（100mg／L）干预。用原位末端标记（TUNEL）法检测细胞凋亡情况，用半定量RT-PCR技术检测凋亡相关基因bcl-2、bax和caspase-3基因mRNA的表达水平。结果10μmol／L Aβ1-40。与海马神经元共孵育24h有明显的细胞毒作用，并可诱导神经元凋亡，加入BFP干预后凋亡指数降低。Aβ1-40可使bcl-2基因表达下调，bax基因表达上调，caspase-3基因的表达增强。加入BFP干预后，部分拮抗了Aβ1-40。诱导的bcl-2基因的表达变化，从而使caspase-3基因的表达降低。结论BFP可通过调控bcl-2／bax的比值、降低caspase-3基因mRNA的表达来阻断Aβ1-40所诱导的海马神经元凋亡，具有神经保护作用。

英文摘要：

Objective To study the protective effects of Bak Foong Pills （BFP） on apoptosis of cultured hippocampus neurons induced by Aβ1-40, and to explore the possible mechanism. Methods Neurotoxicity was measured by MTT method among the cultured hippocampus neurons treated with Aβ1-40 in different concentrations （0. 1 to 30 μmol/L）. Certain concentration of Aβ1-40, which induced the excessive apoptosis of neurons, was determined. Meanwhile, BFP was applied to produce the anti-apoptosis effect. Apoptosis was manifested by TUNEL straining, and the expression levels of bcl-2, bax and caspase-3 were analyzed semi-quantitatively by RT-PCR. Results Significant neurotoxicity was observed after the neurons being incubated with 10 μmol/L Aβ1-40 for 24 h,and then the dose was determined in the study. Excessive apoptosis was observed among the neurons under the same condition, such as down-regulation of bcl-2 expression and up-regulation of bax expression. The apoptotic index （bcl-2/ bax） was reduced, too, which enhanced the expression of caspase-3. Combination of BFP with Aβ1-40 partially corrected the down-regulation of bcl-2 expression. The ratio of bcl-2/bax was increased and the expression of caspase-3 reduced. Conclusion The neuro-protection of BFP might be realized by blocking the apoptosis of hippocampus neurons induce by Aβ1-40, by modulating the ratio of bcl-2/bax and reducing the expression of caspase-3.