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目的：阐明β－ＡＰ诱导神经元凋亡的机制及四氢小檗碱的保护作用。方法：１．形态学观察β－ＡＰ２５－３５诱导离体海马培养神经元凋亡；２．玻片法培养海马神经元，分６组观察四氢小檗碱的保护作用；３．用ＭＴＴ法检测细胞存活情况；４．用Ｆｕｒａ－２技术测定细胞内游离Ｃａ２＋含量。结果：四氢小檗碱组的海马神经元凋亡数量均显著降低（Ｐ＜０．０５），及明显降低β－ＡＰ可诱导细胞内Ｃａ２＋增高，并呈剂量依赖性。结论：四氢小檗碱对神经元凋亡有保护作用，可能与降低细胞内Ｃａ２＋含量有关。
OBJECTIVE: To elucidate the mechanism of β-AP-induced neuronal apoptosis and the protective effect of tetrahydroberberine. Methods: 1. Morphological observation of β-AP25-35 induced apoptosis in cultured hippocampal neurons; 2. Cultured hippocampal neurons by slide method, the protective effects of tetrahydrobiopterin were observed in 6 groups; 3. MTT assay cell survival; 4. Intracellular free Ca2 + content was determined by Fura-2 technique. Results: The apoptosis of hippocampal neurons in tetrahydrobiopterine group was significantly reduced (P <0.05), and significantly decreased in β-AP-induced intracellular Ca2 + in a dose-dependent manner. Conclusion: Tetrahydroberberine has a protective effect on neuronal apoptosis, which may be related to the decrease of intracellular Ca2 + content.