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25C-NBOMe, a Novel Designer Psychedelic, Induces Neurotoxicity 50 Times More Potent Than Methamphetamine In Vitro

Authors
  • Xu, Peng1, 2
  • Qiu, Qiyang2
  • Li, Haijie2
  • Yan, Sicheng2
  • Yang, Mengxiang2
  • Naman, C. Benjamin3
  • Wang, Youmei1
  • Zhou, Wenhua2
  • Shen, Haowei2, 4
  • Cui, Wei2, 3, 4
  • 1 Drug Intelligence and Forensic Center, Ministry of Public Security, Beijing, China , Beijing (China)
  • 2 Ningbo University, Ningbo Key Laboratory of Behavioral Neuroscience, Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo, China , Ningbo (China)
  • 3 Ningbo University, Li Dak Sum Yip Yio Chin Kenneth Li Marine Biopharmaceutical Research Center, College of Food and Pharmaceutical Sciences, Ningbo, China , Ningbo (China)
  • 4 Ningbo University, Department of Physiology, School of Medicine, Ningbo, 315211, China , Ningbo (China)
Type
Published Article
Journal
Neurotoxicity Research
Publisher
Springer-Verlag
Publication Date
Feb 26, 2019
Volume
35
Issue
4
Pages
993–998
Identifiers
DOI: 10.1007/s12640-019-0012-x
Source
Springer Nature
Keywords
License
Yellow

Abstract

25C-NBOMe is a designer substituted phenethylamine and a high-potency psychedelic that acts on the 5-HT2A receptor. Although 25C-NBOMe overdoses have been related to several deaths in the USA and Europe, very limited data exists on the in vitro neurotoxicity of 25C-NBOMe. In this study, we found that 25C-NBOMe potently reduced cell viability of SH-SY5Y, PC12, and SN4741 cells, with IC50 values of 89, 78, and 62 μM, respectively. Methamphetamine decreased the cell viability of these cells with IC50 values at millimolar range in the same tests, indicating that 25C-NBOMe is > 50 times more potent than methamphetamine in its ability to reduce viability of SH-SY5Y cells. The neurotoxicity of 25C-NBOMe on SH-SY5Y cells was further confirmed by using fluorescein diacetate/propidium iodide double staining. 25C-NBOMe elevated the expression of phosphorylated extracellular signal-regulated kinase (pERK), but decreased the expression of phosphorylated Akt and phosphorylated Ser9- glycogen synthase kinase 3β (GSK3β) in time- and concentration-dependent manners. Interestingly, either specific GSK3β inhibitors or specific mitogen-activated protein kinase kinase (MEK) inhibitors significantly prevented 25C-NBOMe-induced neurotoxicity in SH-SY5Y cells. These results suggest that 25C-NBOMe unexpectedly produced more potent neurotoxicity than methamphetamine and that the inhibition of the Akt pathway and activation of the ERK cascade might be involved in 25C-NBOMe-induced neurotoxicity. Most importantly, these findings further inform the toxicity of 25C-NBOMe abuse to the central nervous system for public health.

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