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机构地区:[1]牡丹江医学院,黑龙江牡丹江157011 [2]佳木斯大学,黑龙江佳木斯154007
出 处:《医学综述》2013年第2期346-348,共3页Medical Recapitulate
基 金:黑龙江省教育厅研究生创新科研项目(YJSCX2011-298HLJ)
摘 要:目的研究雌激素对冈田酸诱导的人神经母细胞瘤系(SH-SY5Y)细胞tau蛋白磷酸化的影响。方法四甲基偶氮唑盐观察冈田酸对SH-SY5Y细胞活力的影响,模拟AD时tau蛋白过度磷酸化细胞模型;Western blot检测冈田酸及雌激素对Thr231 tau蛋白磷酸化的影响。结果四甲基偶氮唑盐结果表明,当冈田酸浓度>40 nmol/L时,细胞活力受到明显抑制,<40 nmol/L的冈田酸对细胞活力没有明显的影响;Western blot结果表明,SH-SY5Y细胞经冈田酸处理后,tau蛋白磷酸化的水平明显增加,这种作用可被雌激素所抑制。结论雌激素抑制了冈田酸诱导的SH-SY5Y细胞的tau蛋白磷酸化水平。Objective To study the effect of estrogen on OA-induced SH-SYSY cell hyperphosphoryla- tion of tan protein. Methods MTI" assay was used to observe SH-SYSY cell viability for the preparation of AD tau hyperphosphorylation cell model. Western blot analysis was used to detect the effect of OA and estro- gen on the tan protein phosphorylation level at Thr231 site. Results MTY assay showed that,SH-SY5Y ceil viability was significantly inhibited when OA concentration was greater than 40 nmoL/L, but lower than this concentration OA had no significant effect on cell viability. Westem blot test results showed, SH-SY5Y ceils treated with OA for 12h, tan protein phosphorylation levels were significantly increased, and this effect was in- hibited by estrogen. Conclusion Estrogen can depress the phosphorylation level of tau protein of OA-treated SH-SY5Y cells.
关 键 词:雌激素 TAU蛋白 冈田酸 磷酸化 阿尔茨海默病
分 类 号:R322.81[医药卫生—人体解剖和组织胚胎学]
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