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作 者:万文斌 桑绍明 钟春玖 Wan Wenbin;Sang Shaoming;Zhong Chunjiu(Department of Neurology,Renji Hospital Affiliated to Medical College of Shanghai Jiaotong University,Shanghai,200127,P.R.China;Department of Neurology,Zhongshan Hospital Affiliated to Fudan University,Shanghai,200032,P.R.China)
机构地区:[1]上海交通大学医学院附属仁济医院神经内科,上海200127 [2]复旦大学附属中山医院神经内科,上海200032
出 处:《老年医学与保健》2022年第6期1239-1244,共6页Geriatrics & Health Care
基 金:国家自然科学基金重大研究计划重点项目(91332201);国家重点研发计划“重大慢性非传染性疾病防控研究”重点项目(2016YFC1306400)。
摘 要:目的 观察硫胺素缺乏对小鼠脑内Tau蛋白的影响。方法 小鼠随机分为硫胺素缺乏组和正常对照组,予以造模处理后,提取小鼠皮层及海马脑组织,HPLC测定硫胺素代谢产物含量,蛋白印迹分析总Tau蛋白及其磷酸化水平。结果 与正常对照组比较,硫胺素缺乏组脑内硫胺素代谢物含量显著降低(P<0.01),脑内过度磷酸化Tau蛋白含量显著增加(P<0.01),且Tau蛋白空间构建改变并提示蛋白聚集和难溶性Tau蛋白组分增加(P<0.01)。结论 硫胺素缺乏引起Tau蛋白过度磷酸化及难溶性Tau蛋白水平增加,引起Tau蛋白过度聚集。Objective To observe the effects of thiamine deficiency on Tau protein in mouse brain. Methods Mice were randomly divided into thiamine deficiency group and normal control group. After modeling, the brain tissues of cortex and hippocampus of mice were extracted. The content of thiamine metabolites was determined by HPLC, and total Tau protein and its phosphorylation levels were analyzed by Western blotting. Results Compared with the normal control group, the content of thiamine metabolites in the brain of the thiamine deficiency group decreased significantly(P<0.01), and the content of hyperphosphorylated Tau protein in the brain of the thiamine deficiency group increased significantly(P<0.01), and the Tau protein spatial structure was changed and the protein aggregation and insoluble Tau protein components were increased(P<0.01). Conclusion Thiamine deficiency can cause excessive phosphorylation of Tau protein and increase of insoluble Tau protein content, which will cause excessive aggregation of Tauprotein.
关 键 词:阿尔茨海默病 硫胺素缺乏 脑糖代谢 TAU蛋白 磷酸化
分 类 号:R749.16[医药卫生—神经病学与精神病学]
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