Neuroprotective Effects of Cryptotanshinone in a Direct Reprogramming Model of Parkinson’s Disease

Molecules

HeeMin Yoo¹  JooSeog Yoon²  Kang-Sik Seo²  Joo-Eun Lee³  Mi-Young Son³  Janghwan Kim³  Aruem Baek³  Minhyung Lee³  Young-Joo Jeon³  Hyuna Sim³ 

[1] Group for Biometrology, Korea Research Institute of Standards and Science (KRISS), Daejeon 34113, Korea;Huen Co., Ltd., Gwanggyo Business Center 5F (508), 156, Gwanggyo-ro, Yeongtong-gu, Suwon 16506, Korea;Stem Cell Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Korea;

关键词: Parkinson’s disease;    cryptotanshinone;    disease modeling;    mitochondrial dysfunction;    antioxidant;   

DOI  :  10.3390/molecules25163602

来源: DOAJ

【 摘 要 】

Parkinson’s disease (PD) is a well-known age-related neurodegenerative disease. Considering the vital importance of disease modeling based on reprogramming technology, we adopted direct reprogramming to human-induced neuronal progenitor cells (hiNPCs) for in vitro assessment of potential therapeutics. In this study, we investigated the neuroprotective effects of cryptotanshinone (CTN), which has been reported to have antioxidant properties, through PD patient-derived hiNPCs (PD-iNPCs) model with induced oxidative stress and cell death by the proteasome inhibitor MG132. A cytotoxicity assay showed that CTN possesses anti-apoptotic properties in PD-hiNPCs. CTN treatment significantly reduced cellular apoptosis through mitochondrial restoration, such as the reduction in mitochondrial reactive oxygen species and increments of mitochondrial membrane potential. These effects of CTN are mediated via the nuclear factor erythroid 2-related factor 2 (NRF2) pathway in PD-hiNPCs. Consequently, CTN could be a potential antioxidant reagent for preventing disease-related pathological phenotypes of PD.

【 授权许可】

Unknown