Neuroprotective effects of licochalcone D in oxidative-stress-induced primitive neural stem cells from Parkinson's disease patient-derived iPSCs

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Title
Neuroprotective effects of licochalcone D in oxidative-stress-induced primitive neural stem cells from Parkinson's disease patient-derived iPSCs
Author(s)
Minyoung Oh; Juhyeon Nam; Areum Baek; J H Seo; J I Chae; S Y Lee; S K Chung; Byoung Chul ParkSung Goo ParkJanghwan KimYoung Joo Jeon
Bibliographic Citation
Biomedicines, vol. 11, no. 1, pp. 228-228
Publication Year
2023
Abstract
Parkinson's disease (PD) is one of the most common neurodegenerative diseases caused by the loss of dopaminergic neurons in the substantia nigra pars compacta. Although the etiology of PD is still unclear, the death of dopaminergic neurons during PD progression was revealed to be associated with abnormal aggregation of α-synuclein, elevation of oxidative stress, dysfunction of mitochondrial functions, and increased neuroinflammation. In this study, the effects of Licochalcone D (LCD) on MG132-induced neurotoxicity in primitive neural stem cells (pNSCs) derived from reprogrammed iPSCs were investigated. A cell viability assay showed that LCD had anti-apoptotic properties in MG132-induced oxidative-stressed pNSCs. It was confirmed that apoptosis was reduced in pNSCs treated with LCD through 7-AAD/Annexin Ⅴ staining and cleaved caspase3. These effects of LCD were mediated through an interaction with JunD and through the EGFR/AKT and JNK signaling pathways. These findings suggest that LCD could be a potential antioxidant reagent for preventing disease-related pathological phenotypes of PD.
Keyword
Parkinson’s diseaseInduced pluripotent stem cellsPrimitive neural stem cellsApotosisLicochalcone DJunD
ISSN
2227-9059
Publisher
MDPI
DOI
http://dx.doi.org/10.3390/biomedicines11010228
Type
Article
Appears in Collections:
Division of Research on National Challenges > Stem Cell Convergenece Research Center > 1. Journal Articles
Critical Diseases Diagnostics Convergence Research Center > 1. Journal Articles
Division of Biomedical Research > Disease Target Structure Research Center > 1. Journal Articles
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