Oh Minyoung, Nam Juhyeon, Baek Areum, Seo Ji-Hye, Chae Jung-Il, Lee Seo-Young, Chung Sun-Ku, Park Byoung Chul, Park Sung Goo, Kim Janghwan, Jeon Young-Joo
Stem Cell Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Republic of Korea.
Department of Functional Genomics, KRIBB School of Bioscience, University of Science and Technology, Daejeon 34113, Republic of Korea.
Biomedicines. 2023 Jan 16;11(1):228. doi: 10.3390/biomedicines11010228.
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.
帕金森病（PD）是由黑质致密部多巴胺能神经元缺失引起的最常见的神经退行性疾病之一。尽管PD的病因仍不清楚，但已发现PD进展过程中多巴胺能神经元的死亡与α-突触核蛋白的异常聚集、氧化应激升高、线粒体功能障碍以及神经炎症增加有关。在本研究中，研究了甘草查耳酮D（LCD）对重编程诱导多能干细胞（iPSC）来源的原始神经干细胞（pNSC）中MG132诱导的神经毒性的影响。细胞活力测定表明，LCD在MG132诱导的氧化应激pNSC中具有抗凋亡特性。通过7-AAD/膜联蛋白Ⅴ染色和裂解的caspase3证实，用LCD处理的pNSC中凋亡减少。LCD的这些作用是通过与JunD相互作用以及通过EGFR/AKT和JNK信号通路介导的。这些发现表明，LCD可能是一种潜在的抗氧化剂，用于预防PD的疾病相关病理表型。
