摘要
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 m L/(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）. 〈br〉 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.
出处
《天津医药》
CAS
2016年第9期1088-1091,共4页
Tianjin Medical Journal
基金
漯河医学高等专科学校2015年度基础科学重点研究项目(2015-S-LMC06)
2015年度河南省科技厅基础与前沿技术研究(152300410014)
2014年度河南省科技厅自然科学项目资助(142300410431)
