Show simple item record

dc.contributor.authorKaili Lin
dc.contributor.authorBin Liu
dc.contributor.authorSze-Lam Lim
dc.contributor.authorXiuqiong Fu
dc.contributor.authorStephen C.-W. Sze
dc.contributor.authorKen K.-L. Yung
dc.contributor.authorShiqing Zhang
dc.contributor.otherDepartment of Biology, Faculty of Science, Hong Kong Baptist University (HKBU), Kowloon Tong, Hong Kong Special Administrative Region (HKSAR), China; HKBU Shenzhen Research Institute and Continuing Education, Shenzhen, China
dc.contributor.otherGuangzhou Institute of Cardiovascular Disease, the Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China
dc.contributor.otherDepartment of Biology, Faculty of Science, Hong Kong Baptist University (HKBU), Kowloon Tong, Hong Kong Special Administrative Region (HKSAR), China; HKBU Shenzhen Research Institute and Continuing Education, Shenzhen, China
dc.contributor.otherCenter for Cancer and Inflammation Research, School of Chinese Medicine, HKBU, Kowloon Tong, HKSAR, China
dc.contributor.otherDepartment of Biology, Faculty of Science, Hong Kong Baptist University (HKBU), Kowloon Tong, Hong Kong Special Administrative Region (HKSAR), China; HKBU Shenzhen Research Institute and Continuing Education, Shenzhen, China
dc.contributor.otherDepartment of Biology, Faculty of Science, Hong Kong Baptist University (HKBU), Kowloon Tong, Hong Kong Special Administrative Region (HKSAR), China; HKBU Shenzhen Research Institute and Continuing Education, Shenzhen, China; Corresponding author. Department of Biology, Faculty of Science, Hong Kong Baptist University (HKBU), Kowloon Tong, Hong Kong Special Administrative Region (HKSAR), China
dc.contributor.otherDepartment of Biology, Faculty of Science, Hong Kong Baptist University (HKBU), Kowloon Tong, Hong Kong Special Administrative Region (HKSAR), China; HKBU Shenzhen Research Institute and Continuing Education, Shenzhen, China; Corresponding author. Department of Biology, Faculty of Science, Hong Kong Baptist University (HKBU), Kowloon Tong, Hong Kong Special Administrative Region (HKSAR), China
dc.date.accessioned2020-05-01T05:10:35Z
dc.date.available2025-10-02T03:04:22Z
dc.date.issued01-05-2020
dc.identifier.issn-
dc.identifier.urihttp://www.sciencedirect.com/science/article/pii/S1226845318302525
dc.description.abstractBackground: Active natural ingredients, especially small molecules, have recently received wide attention as modifiers used to treat neurodegenerative disease by promoting neurogenic regeneration of neural stem cell (NSC) in situ. 20(S)-protopanaxadiol (PPD), one of the bioactive ingredients in ginseng, possesses neuroprotective properties. However, the effect of PPD on NSC proliferation and differentiation and its mechanism of action are incompletely understood. Methods: In this study, we investigated the impact of PPD on NSC proliferation and neuronal lineage differentiation through activation of the Wnt/glycogen synthase kinase (GSK)-3β/β-catenin pathway. NSC migration and proliferation were investigated by neurosphere assay, Cell Counting Kit-8 assay, and EdU assay. NSC differentiation was analyzed by Western blot and immunofluorescence staining. Involvement of the Wnt/GSK3β/β-catenin pathway was examined by molecular simulation and Western blot and verified using gene transfection. Results: PPD significantly promoted neural migration and induced a significant increase in NSC proliferation in a time- and dose-dependent manner. Furthermore, a remarkable increase in antimicrotubule-associated protein 2 expression and decrease in nestin protein expression were induced by PPD. During the differentiation process, PPD targeted and stimulated the phosphorylation of GSK-3β at Ser9 and the active forms of β-catenin, resulting in activation of the Wnt/GSK-3β/β-catenin pathway. Transfection of NSCs with a constitutively active GSK-3β mutant at S9A significantly hampered the proliferation and neural differentiation mediated by PPD. Conclusion: PPD promotes NSC proliferation and neural differentiation in vitro via activation of the Wnt/GSK-3β/β-catenin pathway by targeting GSK-3β, potentially having great significance for the treatment of neurodegenerative diseases. Keywords: 20(S)-protopanaxadiol, Neural differentiation, Neural stem cell, Proliferation, Wnt/GSK-3β/β-catenin pathway
dc.format-
dc.language.isoEN
dc.publisherElsevier
dc.relation.uri['https://www.fssp.uaic.ro/argumentum/Argumentum%20en.htm', 'https://www.fssp.uaic.ro/argumentum/Submission%20Guidelines.pdf', 'https://www.fssp.uaic.ro/argumentum/']
dc.rightsCC BY-ND
dc.subject['logic', 'argumentation', 'rhetoric', 'philosophy', 'communication', 'Language and Literature', 'P', 'Oral communication. Speech', 'P95-95.6', 'Language. Linguistic theory. Comparative grammar', 'P101-410']
dc.subject.lccBotany
dc.title20(S)-protopanaxadiol promotes the migration, proliferation, and differentiation of neural stem cells by targeting GSK-3β in the Wnt/GSK-3β/β-catenin pathway
dc.typeArticle
dc.description.pages475-482
dc.description.doi10.1016/j.jgr.2019.03.001
dc.title.journalJournal of Ginseng Research
dc.identifier.e-issn-
dc.identifier.oaioai:doaj.org/journal:11d95192759441d78758962168af4dab
dc.journal.infoVolume 44, Issue 3


This item appears in the following Collection(s)

Show simple item record