中文摘要：

目的观察蛇床子素对β淀粉样蛋白25-35片段（Aβ25-35）诱导大鼠神经毒性的影响。并研究其可能机制。方法将30只雄性SD大鼠随机分为3组：假手术组、模型组和治疗组（n=10）。双侧海马注射Aβ25-35制模后,治疗组每日1次灌胃蛇床子素40 mg/kg,假手术组和模型组灌胃等体积溶媒,连续15 d后处死大鼠,每组随机取3只行HE染色观察神经元损伤情况,其余大鼠分别采用Western blot法检测IL-1β、TNF-α蛋白表达及p-NF-κB p65水平。结果模型组大鼠海马CA1区神经元较假手术组明显受损,且IL-1β、TNF-α蛋白表达及p-NF-κB p65水平增加（P〈0.01）;然而,蛇床子素减轻了Aβ25-35诱导的神经元损伤,降低了IL-1β（P〈0.05）、TNF-α蛋白表达及p-NF-κB p65水平（P〈0.01）。结论蛇床子素抑制NF-κB的激活,下调IL-1β、TNF-α蛋白表达,可能是其轻减Aβ25-35所致大鼠神经元损伤的机制之一。

英文摘要：

Objective This study was designed to investigate the effect of osthole on neurotoxicity induced by β - amyloid 25 - 35 in rats, and explore its potential mechanisms. Methods Male Sprague - Dawley rats were randomly divided into three groups： sham group, model group and osthole -treated group. The rat model of neurotoxicity was induced by injecting Aβ26-35 into the bilateral hippocampus. Then treated groups were administrated with osthole （40 mg/kg per day, po） for 15 d, while rats in sham and model groups were administrated with volume-matched vehicle. Hippocampal neuronal injury was observed by Haematoxylin- Eosin staining and the protein expressions of IL - 1β, TNF -α, and the level of p - NF - κB p65, were detected by Western blot . Results Administration of Aβ25-35 to bilateral hippocampus significantly caused neuronal injury in CA1 region, and increased the protein expression of IL - 1β, TNF - α, and the level of p - NF -κB p65 compared with those in sham operation group （P 〈 0.01 ）. However, treatment with osthole significantly attenuated neuronal injury and reduced the protein expression of IL - 1β （ P 〈 0.05 ） , TNF - α, and the level of p - NF - κB p65 compared with model group （P 〈 0.01 ）. Conclusion Osthole attenuates neuronal injury induced by Aβ25-35 in rats through suppressing NF - κB activation, reducing the protein expression of IL - 1β, and TNF -α.