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机构地区:[1]南通大学医学院药理学系,南通226001 [2]南通大学附属医院神经内科
出 处:《南通大学学报(医学版)》2013年第3期169-171,共3页Journal of Nantong University(Medical sciences)
基 金:南通市应用研究科技计划项目(BK2011042)
摘 要:目的:观察血清饥饿对HT22细胞叉头框蛋白O1(forkhead box protein O1,FOXO1)蛋白表达的影响,探讨FOXO1蛋白在脑缺血损伤中的意义。方法:建立去血清饥饿损伤细胞模型,乳酸脱氢酶(lactate dehydrogenase,LDH)法检测细胞损伤,四甲基偶氮盐(methylthiazolyl tetrazolium,MTT)法检测细胞活力;Western Blot检测血清饥饿对HT22细胞FOXO1蛋白磷酸化的影响。结果:LDH和MTT结果显示随着血清饥饿时间的延长,细胞损伤增加,细胞活力逐渐下降,呈时间依赖性。去血清饥饿6 h后,FOXO1的Ser 319位点磷酸化降低,Ser256和Thr24位点的磷酸化水平增加。结论:血清饥饿诱导的神经元损伤可以导致FOXO1蛋白的磷酸化水平发生变化。Objective: To investgate the expression levels of forkhead box protein O1(FOXO1) in HT22 cells after serum starvation injury and explore the significance of FOXO1 protein in the cerebral ischemic injury.Methods: To build an serum starvation model of HT22 cells,lactate dehydrogenase(LDH) assay was used to detect the degree of cell damage,and methylthiazolyl tetrazolium(MTT) assay was applied to detect cell viability.Western Blot was used to investigate the effect of serum starvation on the alteration of FOXO1 phosphorylation in HT22 cells.Results: The results of LDH and MTT assay indicated that serum starvation could evoke cell damage and decrease cell viability in a time-dependent manner.Starvation stimulation for 6 h could reduce FOXO1 phosphorylation at Ser 319,while increase FOXO1 phosphorylation at Ser 256 and Thr 24.Conclusion: The neuronal damage induced by serum starvation could result in the changes of the phosphorylation level of FOXO1 protein.
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