文献类型：期刊文献

中文题名：阿魏酸对Aβ25-35诱导PC12细胞的保护机制研究

英文题名：Protection Effect of Ferulic Acid to PC12 Nerve Cells Induced by Aβ25-35

作者：杨长生[1];杨植媛[2];吴红彦[1,2];李海龙[1,2];吴亚娜[2]

第一作者：杨长生

机构：[1]甘肃中医学院,甘肃兰州730000;[2]甘肃省中医方药挖掘与创新转化重点实验室,甘肃省中药新产品创制省级工程实验室,甘肃兰州730000

第一机构：甘肃中医药大学

年份：2015

卷号：42

期号：1

起止页码：33

中文期刊名：辽宁中医杂志

外文期刊名：Liaoning Journal of Traditional Chinese Medicine

收录：CSTPCD;;北大核心:【北大核心2014】；

基金：国家自然科学基金项目(81060284)

语种：中文

中文关键词：阿尔兹海默病;阿魏酸;β-淀粉样蛋白25-35(Aβ25-35)

外文关键词：Alzheimer disease; Ferulic acid; β-amyloid peptide25-35

摘要：目的:观察阿魏酸对β-淀粉样蛋白25-35(βamyloid peptide25-35,Aβ25-35)诱导的阿尔兹海默病(Alzheimer disease,AD)模型细胞的抗氧化能力的影响,探讨当归防治AD的作用及机制。方法:用Aβ25-35诱导PC12细胞凋亡,以不同浓度阿魏酸对抗干预,以MTT比色法观测阿魏酸对AD模型细胞增殖的保护作用,以比色法检测阿魏酸对AD模型细胞培养液中超氧化物歧化酶(SOD)、丙二醛(MDA)、乳酸脱氢酶(LDH)的影响。用RT-PCR法检测Apbb1,乙酰胆碱酯酶(Ache)基因的表达。结果:阿魏酸对损伤的PC12细胞的存活率有提高作用,阿魏酸在2 mmol/L时可明显降低模型细胞培养液中MDA、LDH含量,提高SOD活力,差异有统计学意义(P<0.01)。阿魏酸可下调Apbb1和Ache的mRNA表达,差异有统计学意义(P<0.01)。结论:阿魏酸对Aβ25-35损伤的PC12细胞有保护作用,机制可能与提高细胞抗氧化能力相关,与下调Apbb1、Ache的mRNA表达量相关。
Objective： To observe the effect of Ferulic acid to the antioxidant capacity of model cell induced by Aβ25-35. To explore the effect and mechanism of angelica prevention and treatment of AD. Methods： We separately induced PC12 cells by using Aβ25-35 to against and intervened Ferulic acid with different concentration. MTT colorimetric method was used to detect and observation protection effect of Ferulic acid to cell proliferation on two kinds of AD models. Colorimetric method was used to detect the influence of Ferulic acid to activity of lactic dehydrogenase,MDA content,SOD activity and LDH content in damaged PC12 cell culture. We explored the gene expression of Apbb1 and Ache by RT-pcr method. Results： Ferulic acid increased the survival rate of damaged PC12 cells and the peak was at 2 mmol / L in Aβ25-35 models which can obviously decrease MDA content and improve SOD activity（ P〈0. 01）. Ferulic acid can cut mRNA expression of Ache and Apbb1（ P〈0. 01）. Conclusion： Ferulic acid can prevent PC12 cell from ability of the cell and Ache and mRNA expression of Ache and Apbb1.