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Zeaxanthin Attenuates the Vicious Circle Between Endoplasmic Reticulum Stress and Tau Phosphorylation: Involvement of GSK-3 beta Activation  ( SCI-EXPANDED收录)  

文献类型:期刊文献

英文题名:Zeaxanthin Attenuates the Vicious Circle Between Endoplasmic Reticulum Stress and Tau Phosphorylation: Involvement of GSK-3 beta Activation

作者:Zhang, Li-Na[1,2,3];Li, Meng-Jie[1,2,3];Shang, Ying-Hui[1,2,3];Liu, Yun-Ru[1,2,3];Han-Chang, Huang[1,2,3];Lao, Feng-Xue[1,2,3]

通讯作者:Lao, FX[1]

机构:[1]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing, Peoples R China;[2]Beijing Union Univ, Inst Funct Factors & Brain Sci, Beijing, Peoples R China;[3]Beijing Union Univ, Coll Biochem Engn, Beijing, Peoples R China

第一机构:北京联合大学应用文理学院|北京联合大学生物化学工程学院

通讯机构:[1]corresponding author), Beijing Union Univ, Inst Funct Factors & Brain Sci, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China.|[114172]北京联合大学应用文理学院;[11417]北京联合大学;[1141726]北京联合大学生物化学工程学院;

年份:2022

卷号:86

期号:1

起止页码:191-204

外文期刊名:JOURNAL OF ALZHEIMERS DISEASE

收录:;Scopus(收录号:2-s2.0-85126389313);WOS:【SCI-EXPANDED(收录号:WOS:000768536700008)】;

基金:The authors are grateful to Beijing Key Laboratory of Bioactive Substances and Functional Food and the Institute of Functional Factors and Brain Science. This work was supported by the National Natural Science Foundation of China (31471587), and the Academic Research Projects of Beijing Union University (ZK40201902, JZ10202001, XP202008). Authors' disclosures available online (https://www.j-alz.com/manuscript-disclosures/21-5408r2).

语种:英文

外文关键词:Alzheimer's disease; glycogen synthase kinase 3 beta; SB216763; tau; Zeaxanthin

摘要:Background: Alzheimer's disease (AD) characterized by neurofibrillary tangles caused by hyperphosphorylated tau is the most common cause of dementia. Zeaxanthin (Zea), derived from fruits and vegetables, may reduce the risk of AD. Endoplasmic reticulum stress (ERS) might cause memory impairment in AD. Objective: Here, we studied protective role of Zea on the relationship among ERS, activity of glycogen synthase kinase 3 beta (GSK-3 beta, tau phosphorylated kinase), and p-Tau (Ser 396 and Thr 231). Methods: The results were obtained in non-RA and RA group by using different treatment, such as 9-cis-retinoic acid (RA), TM (ERS inducer), Zea, 4-PBA (ERS inhibitor), and SB216763 (GSK-3 beta inhibitor). The methods included flow cytometry and MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] for the detections of cell cycle and cell viability and western blot as a third measure of proteins in relation to ERS and tau phosphorylation. We have collected and analyzed all the data that suggested application of drugs for the treatment in non-RA and RA group. Results: Zea displays its protection on TM-induced cell injury, upregulation of GRP78 expression, and change of GSK-3 beta activity and tau phosphorylation when 4-PBA and SB216763 interfere with the process. Conclusion: These studies indicated that Zea is in vicious circle in ERS, GSK-3 beta, and tau phosphorylation, and further reflect its potential value in AD.

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