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作 者:胡江平[1] 蔡克瑞[1] 金花淑[1] 金在顺[1] 李凯军[1]
机构地区:[1]牡丹江医学院组织胚胎学教研室,黑龙江牡丹江157011
出 处:《中风与神经疾病杂志》2014年第4期332-334,共3页Journal of Apoplexy and Nervous Diseases
基 金:黑龙江省教育厅海外学人项目(1153h16);牡丹江医学院科技项目(ZS201329;ZS201303)
摘 要:目的研究丙戊酸钠(VPA)对冈田酸(OA)处理的人神经母细胞瘤系(SH-SY5Y)细胞中tau蛋白磷酸化的影响。方法 MTT观察OA对SH-SY5Y细胞活力的影响,制备tau蛋白过度磷酸化的细胞模型;Western blot检测OA及VPA对Thr231位点tau蛋白磷酸化的影响。结果 MTT结果显示,当OA浓度大于40 nmol/L时,细胞活力受到明显抑制,而低于此浓度的OA对细胞活力的影响不明显;Western blotting结果显示,SH-SY5Y细胞经OA(40 nmol/L,12 h)处理后,Tau蛋白磷酸化的水平明显增加,给予VPA(10 mmol/L)作用12 h后,Tau蛋白磷酸化的水平明显下降。结论 VPA可以抑制OA处理的SH-SY5Y细胞的tau蛋白过度磷酸化。Objective To study the inhibition of VPA on OA-induced SH-SY5Y cell hyperphosphorylation of tau protein. Methods We observed SH-SY5Y cell viability by MTT assay for the preparation of AD tau hyperphosphorylation cell model. We detected the effects of OA and VPA on the tau protein phosphorylation level at Thr231 site by Western blotting analysis. Results MTT assay showed that,when OA concentration was higher than 40 nmol/L, SH-SY5Y cell viability was significantly inhibited, whereas lower than this concentration, there was no significant effect on cell viability. Western blotting showed that, Tau protein phosphorylation levels of SH-SY5Y cells were significantly increased after OA treatment for 12 h,the effect of which was inhibited by VPA. Conclusion VPA can inhibit the phosphorylation level of tau protein in OA-treated cells.
关 键 词:VPA TAU蛋白 冈田酸 磷酸化 阿尔茨海默病
分 类 号:R749.1[医药卫生—神经病学与精神病学]
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