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Estrogen improves sevoflurane-induced cognitive dysfunction by regulating synaptic zinc homeostasis
Feixiang Li1, Bingqing Gong1, Tao Yang2
1Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin Institute of Anesthesiology, NO.154, Anshan Road, Heping District, Tianjin, 300052, China.
Molecular Medicine (Cambridge, Mass.)
|October 14, 2025
Summary
Sevoflurane anesthesia disrupts synaptic zinc balance, causing cognitive dysfunction. Estrogen protects the brain by restoring this zinc homeostasis, offering potential perioperative neuroprotection.
Area of Science:
- Neuroscience
- Anesthesiology
- Pharmacology
Background:
- Sevoflurane anesthesia is linked to cognitive dysfunction, with unclear mechanisms.
- Synaptic zinc homeostasis disruption is implicated in neurotoxicity and cognitive impairment.
Purpose of the Study:
- Investigate synaptic zinc imbalance in sevoflurane-induced cognitive dysfunction.
- Evaluate estrogen's neuroprotective effects against sevoflurane neurotoxicity.
Main Methods:
- Aged female mice exposed to sevoflurane.
- Assessed synaptic zinc, Tau phosphorylation, synaptic vesicles, neuronal firing, and damage.
- Evaluated effects of zinc chelation (CaEDTA) and estrogen on cognitive function (Morris water maze, Y-maze).
Main Results:
- Sevoflurane disrupted zinc homeostasis via Znt3 upregulation, increasing Tau phosphorylation, reducing vesicles/firing, causing neuronal death, and impairing cognition.
- CaEDTA chelation attenuated Tau phosphorylation/neuronal death, enhanced firing, and improved cognition.
- Estrogen downregulated Znt3, alleviating zinc imbalance, reducing Tau phosphorylation/neuronal loss, and improving cognitive function.
Conclusions:
- Sevoflurane-induced cognitive dysfunction is linked to synaptic zinc imbalance.
- Estrogen protects neurons by restoring synaptic zinc homeostasis.
- Findings suggest estrogen's therapeutic potential in preventing anesthesia-related cognitive impairment.
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