[1]孙上奇 刘聪聪 田野等.2,5-二叔丁基对苯二酚对阿尔茨海默病细胞模型的保护作用[J].卒中与神经疾病杂志,2022,29(01):3-7.[doi:10.3969/j.issn.1007-0478.2022.01.001]
　Sun Shangqi,Liu Congcong,Tian Ye,et al.Protective effect of 2,5-Di-tert-butylhydroquinone on cellular models of Alzheimer’s disease[J].Stroke and Nervous Diseases,2022,29(01):3-7.[doi:10.3969/j.issn.1007-0478.2022.01.001]
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2,5-二叔丁基对苯二酚对阿尔茨海默病细胞模型的保护作用()
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《卒中与神经疾病》杂志[ISSN:1007-0478/CN:42-1402/R]

卷:
第29卷
期数:
2022年01期
页码:
3-7
栏目:
论 著
出版日期:
2022-02-15

文章信息/Info

Title:
Protective effect of 2,5-Di-tert-butylhydroquinone on cellular models of Alzheimer’s disease
文章编号:
1007-0478(2022)01-0003-06
作者:
孙上奇 刘聪聪 田野等
430060 武汉大学人民医院神经内科[孙上奇 刘聪聪 田野 张兆辉 张振涛(通信作者)]
Author(s):
Sun Shangqi;  Liu Congcong;  Tian Ye;  et al
Department of Neurology, Renmin Hospital of Wuhan University, Wuhan Hubei 430060
关键词:
2; 5-二叔丁基对苯二酚 阿尔茨海默病 氧化应激 线粒体
Keywords:
2; 5-Di-tert-butylhydroquinone Alzheimer’s disease Oxidative stress Mitochondria
分类号:
R742
DOI:
10.3969/j.issn.1007-0478.2022.01.001
文献标志码:
A
摘要:
目的 探讨2,5-二叔丁基对苯二酚(2,5-Di-tert-butylhydroquinone,DBHQ)对阿尔茨海默病细胞模型的保护作用及分子机制。方法 利用K18聚集体处理稳定转染Tau片段的HEK293细胞,制作Tau蛋白聚集的细胞模型; 利用DBHQ处理细胞,荧光显微镜检测DBHQ对Tau蛋白聚集的影响; 在HT22神经元中转导K18聚集体,光镜下观察DBHQ对HT22细胞形态的影响; 用DCFH-DA探针及DHE探针检测DBHQ对活性氧和超氧阴离子的影响; 在HT22细胞中转染mito-Dendra2质粒,共聚焦显微镜动态记录线粒体融合功能。结果 K18聚集体诱导细胞内Tau蛋白聚集,而DBHQ可以减轻K18聚集体诱导的Tau蛋白聚集; K18聚集体处理后HT22细胞发生形态改变,而DBHQ减轻K18诱导的细胞形态变化,并降低细胞内活性氧和超氧阴离子水平; 线粒体融合功能检测发现DBHQ增强线粒体功能。结论 本研究表明DBHQ可减少细胞内的Tau蛋白聚集,并保护线粒体、减轻氧化应激水平,对阿尔茨海默病细胞模型起到保护作用。
Abstract:
Objective To explore the protective effect and molecular mechanisms of 2,5-di-tert-butylhydroquinone(DBHQ)on cellular models of Alzheimer’s disease.Methods K18 fibrils were used to treat HEK293 cells stably transfected with tau fragments to make a cellular model of tau aggregation. The effect of DBHQ on tau aggregation was detected by fluorescence microscope. The effect of DBHQ on the morphology of K18 fibrils-treated HT22 cells in the presence or absence of DBHQ were observed under a light microscope. DCFH-DA probe and DHE probe were used to detect the effect of DBHQ on the levels of reactive oxygen species and superoxide anion. To observe the effect of DBHQ on mitochondrial function, the HT22 cells were transfected with mito-Dendra2 plasmid. The mitochondrial fusion function was dynamically recorded by a confocal microscope.Results K18 fibrils induced tau aggregation, while DBHQ reduced the aggregation of tau. Besides, DBHQ attenuated K18-induced cell morphological changes of HT22 cells, and decreased the levels of reactive oxygen species and superoxide anionsin HT22 cells. The mitochondrial fusion function test found that DBHQ protected mitochondrial function from the toxicity of K18 fibrils.Conclusion Our results indicate that DBHQ alleviates the accumulation of tau in cells. It attenuates mitochondrial dysfunction, reduces oxidative stress, and plays a protective role in the cellular models of Alzheimer’s disease.

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备注/Memo

备注/Memo:
基金项目:国家自然科学基金(No.81822016、81771382)
更新日期/Last Update: 1900-01-01