Ethanol inhibition of undifferentiated rat neural progenitor cell replication can be prevented by chlorogenic acid via the NFATc4/CSE signalling pathway.

These findings demonstrate that EtOH can perturb CSE-dependent redox homeostasis via impairing the NFATc4 signalling pathway in neuroblasts. Notably, EtOH-associated impairments were rescued by genetic or pharmacological activation of NFATc4. Further, we report a potential role for CGA in mitigating the EtOH-related neuroblast toxicity with a compelling connection to the NFATc4/CSE pathway.