Version 1
: Received: 3 May 2024 / Approved: 7 May 2024 / Online: 7 May 2024 (11:48:13 CEST)
How to cite:
Leow, D. M. K.; Cheah, I. K. M.; Chen, L.; Ng, Y. K.; Yeo, C. J. J.; Halliwell, B.; Ong, W. Y. Ergothioneine Mediated Neuroprotection of Human iPSC derived-Dopaminergic Neurons.. Preprints2024, 2024050382. https://doi.org/10.20944/preprints202405.0382.v1
Leow, D. M. K.; Cheah, I. K. M.; Chen, L.; Ng, Y. K.; Yeo, C. J. J.; Halliwell, B.; Ong, W. Y. Ergothioneine Mediated Neuroprotection of Human iPSC derived-Dopaminergic Neurons.. Preprints 2024, 2024050382. https://doi.org/10.20944/preprints202405.0382.v1
Leow, D. M. K.; Cheah, I. K. M.; Chen, L.; Ng, Y. K.; Yeo, C. J. J.; Halliwell, B.; Ong, W. Y. Ergothioneine Mediated Neuroprotection of Human iPSC derived-Dopaminergic Neurons.. Preprints2024, 2024050382. https://doi.org/10.20944/preprints202405.0382.v1
APA Style
Leow, D. M. K., Cheah, I. K. M., Chen, L., Ng, Y. K., Yeo, C. J. J., Halliwell, B., & Ong, W. Y. (2024). Ergothioneine Mediated Neuroprotection of Human iPSC derived-Dopaminergic Neurons.. Preprints. https://doi.org/10.20944/preprints202405.0382.v1
Chicago/Turabian Style
Leow, D. M. K., Barry Halliwell and Wei Yi Ong. 2024 "Ergothioneine Mediated Neuroprotection of Human iPSC derived-Dopaminergic Neurons." Preprints. https://doi.org/10.20944/preprints202405.0382.v1
Abstract
Oxidative stress-mediated cell death is a major cause of dopaminergic neuronal loss in the substantia nigra (SN) of Parkinson’s disease patients. Ergothioneine (ET), a natural dietary compound, has been shown to have cytoprotective functions, but neuroprotective actions against PD have not been well established. 6-Hydroxydopamine (6-OHDA) is a widely used neurotoxin to simulate the degeneration of dopaminergic (DA) neurons in Parkinson's disease. In this study, we investigated the protective effect of ET on 6-OHDA treated iPSC-derived dopaminergic neurons (iDAs) and further confirmed the protective effects in 6-OHDA treated human neuroblastoma SH-SY5Y cells. In 6-OHDA treated cells, metabolic stress in the form of decreased mitochondrial membrane potential (ΔΨm), increased mitochondrial reactive oxygen species (mROS), reduced cellular ATP levels, and increased total protein carbonylation levels was observed. 6-OHDA treatment also significantly decreased tyrosine hydroxylase levels. These effects were significantly abrogated when ET was present. Verapamil hydrochloride (VHCL), a non-specific inhibitor of the ET transporter, OCTN1, abolished ET’s cytoprotective effects, indicative of an intracellular action. These results suggest that ET could be a potential therapeutic for Parkinson’s disease.
Biology and Life Sciences, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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