原儿茶酸对Aβ_(1-42)寡聚体诱导AD海马神经元的保护作用  

Protective effect of protocatechuic acid on AD hippocampl neurons treated with Aβ_(1-42) oligomer

作　　者：李智勇[1] 罗汉[1] 张海英[2] 

机构地区：[1]海口市人民医院神经外科,海南海口570208 [2]海南医学院人体解剖学教研室,海南海口571101

出　　处：《海南医学》2015年第14期2029-2031,共3页Hainan Medical Journal

基　　金：国家自然科学基金(编号:81100246);海南省自然科学基金(编号:811204);海口市重点科技计划项目(编号:2011-0135)

摘　　要：目的应用Aβ1-42寡聚体诱导SD胎鼠海马神经元制备细胞损伤模型,观察海南益智仁提取物-原儿茶酸(PCA)对模型细胞的保护作用。方法采用四甲基偶氮唑盐微量酶反应比色法(MTT法)检测细胞活力,流式细胞技术检测细胞凋亡,蛋白质印迹法(Western blot)检测ERK蛋白,观察原儿茶酸对模型细胞的保护作用。结果 Aβ1-42寡聚体干预SD胎鼠海马神经元后,神经元生存率下降,神经元凋亡率升高,ERK蛋白表达下调。添加原儿茶酸后,模型细胞存活率改善明显、凋亡率显著性降低,且呈现浓度依赖性,并且ERK蛋白表达上调。结论原儿茶酸可拮抗Aβ1-42寡聚体所诱导的海马神经元损伤,具有神经保护作用。Objective To study the effect of protocatechuic acid（PCA） from Alpinia oxyphylla in Hainan on nerve cell injury models, which were established by incubating hippocampl neurons of SD fetal rats in the presence ofβ-amyloid 1-42（Aβ1-42） oligomer. Methods With cell viability detected by MTT, apoptosis detected by flow cytometry and ERK protein detected by Western blot, the protective effect of PCA on nerve cell injury models was observed.Results After intervention by Aβ1-42 oligomer. the viability of hippocampl neurons were decreased; The apoptotic rate increased; ERK protein expression was down-regulated. However, after the addition of PCA, the viability of hippocampl neurons significantly improved and the apoptotic rate significantly reduced, with dose-dependent effect. The expression of ERK protein was also up-regulated. Conclusion PCA had a significant protective effect against A β1-42oligomer-induced injury.

关 键 词：阿尔茨海默病 Aβ1-42寡聚体 原儿茶酸 ERK信号通路 

分 类 号：R332[医药卫生—人体生理学]