Tier 3 — preclinical

Betaine alleviates neuronal impairment in glutamate-injured SH-SY5Y neuroblastoma cells via Nrf2 signaling pathway related ferroptosis

Guihua Wu, Fuwei Wang, Zihao Chen, Nan Zheng, Qiong Zhou, Lihua Xie, Xinyu Yang, Daibo Song, Qiang Sun, Jiantao Lin, Li Li
Journal of neuroimmunology 2026 414:578886

Bibliography

PubMed
PMID 41707471
Funding
Funding was not specified in the indexed record or accessible funding metadata.
Competing interests
Reported disclosure: The authors declare no conflict of interests.

Study snapshot

DesignExperimental animal and/or laboratory research
ModelSH-SY5Y neuroblastoma cells
SampleExperiment-specific biological replicates and model groups; see original methods
InterventionBetaine during glutamate-induced cellular injury
DurationIn vitro exposure
EndpointsCell survival; Ferroptosis; Nrf2

What the study showed, in plain terms

Published in 2026, this source examined preclinical aging, brain and metabolic mechanisms. Design: Experimental animal and/or laboratory research. Sample/model: Experiment-specific biological replicates and model groups; see original methods. The exposure or intervention was Betaine during glutamate-induced cellular injury. Follow-up or treatment period: In vitro exposure.

Betaine improved viability and selected ferroptosis/oxidative-stress markers, alongside Nrf2-related changes.

Experimental model evidence. The intervention, concentrations and outcomes do not establish an effective human supplement dose or a clinical treatment benefit.

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Key findings

  • Betaine improved viability and selected ferroptosis/oxidative-stress markers, alongside Nrf2-related changes.
  • The recorded outcome domains were Cell survival; Ferroptosis; Nrf2.
  • The result applies to the tested exposure: Betaine during glutamate-induced cellular injury; In vitro exposure.

What this study can and cannot tell us

  • Experimental model evidence. The intervention, concentrations and outcomes do not establish an effective human supplement dose or a clinical treatment benefit.
  • Cell concentrations, species, disease models and experimental routes cannot be converted directly into an effective or safe oral human regimen.
  • Source basis: Indexed abstract and bibliographic data. Missing method details, funding information or participant denominators are not inferred.

Editorial review

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