目的：观察美满霉素对阿尔茨海默病（AD）大鼠认知功能和海马脑源性神经营养因子（BDNF）、凋亡相关因子Bcl-2和Bax表达的影响，探讨美满霉素对AD大鼠脑保护作用的机制。方法侧脑室注射Aβ25-35建立AD大鼠模型。30只健康雄性SD大鼠随机分成对照组、模型组和治疗组，每组10只。对照组和模型组腹腔内注射生理盐水1 mL/（kg·d），治疗组腹腔注射美满霉素50 mg/（kg·d），均持续14 d。Morris水迷宫检测行为学变化，蛋白免疫印迹（Western blotting）法和酶联免疫吸附试验（ELISA）法检测海马BDNF、Bcl-2和Bax蛋白的表达，原位末端标记（TUNEL）法检测海马神经元凋亡率。结果美满霉素可以明显提高AD大鼠学习记忆能力，上调AD大鼠海马BDNF、Bcl-2表达，下调Bax表达，减少海马神经元凋亡。结论美满美素可以通过促进神经元的生长、抑制神经元的凋亡发挥脑保护作用。%Objective To investigate the effect of minocycline on the cognition and expressions of brain-derived neurotrophic factor (BDNF), apoptosis related factor Bcl-2 and Bax in hippocampus of rats with Alzheimer’s disease (AD). Methods The rat model was established by microinjection of Aβ25-35 into lateral ventricle. Thirty healthy male SD rats were randomly divided into three groups:control group, model group and minocycline treatment group. Normal saline 1 mL/(kg·d) was intraperitoneally injected in control group and model group. The minocycline treatment group was intraperitoneally injected with minocycline 50 mg/(kg · d) for 14 days. Morris water maze was used to detect the behaviors of animals. The expressions of BDNF, Bcl-2 and Bax in hippocampus were measured by Western blotting and enzyme linked immunosorbent assay (ELISA). The apoptosis of neurons was detected by TdT-mediated dUTP nick-end labeling (TUNEL). Results Minocycline greatly improved the behaviors of AD rats, up-regulated the expressions of BDNF and Bcl-2, and down-regulated the expression of Bax in hippocampus, and reduced cell apoptosis. Conclusion Minocycline plays a protective role in neural function by promoting the growth of neurons and inhibiting the neuronal apoptosis.
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