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MitoQ reducing sevoflurane-induced cognitive dysfunction by modulating mitochondrial dysfunction.

Hengjie Su1, Zhibin He2, Haotian Wu2

  • 1Chinese Academy of Medical Sciences & Peking Union Medical College, Institute of Biomedical Engineering, Beijing, China.

Metabolic Brain Disease
|October 30, 2025
PubMed
Summary
This summary is machine-generated.

Mitoquinone (mitoQ) treatment prevented sevoflurane-induced cognitive decline in aged mice by reducing oxidative stress, inflammation, and apoptosis. This antioxidant therapy offers potential for preventing postoperative neurocognitive disorders (POCD).

Keywords:
MitochondriaMitoquinone (MitoQ)Postoperative cognitive complications

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Area of Science:

  • Neuroscience
  • Anesthesiology
  • Gerontology

Background:

  • Postoperative neurocognitive disorders (POCD) are common complications impacting patient quality of life.
  • Perioperative anesthesia exposure, particularly sevoflurane, is a key factor contributing to POCD.
  • Mitoquinone (mitoQ), a mitochondrial-targeted antioxidant, is investigated for its therapeutic potential.

Purpose of the Study:

  • To investigate the therapeutic effect of mitoQ in counteracting sevoflurane-induced cognitive dysfunction.
  • To explore the mechanisms underlying sevoflurane's impact on cognitive function and mitoQ's protective effects.

Main Methods:

  • Aged male mice were treated with mitoQ before sevoflurane exposure.
  • Spatial learning ability was assessed using a water maze.
  • Mitochondrial function, oxidative stress, inflammation, autophagy, and apoptosis were analyzed in brain tissues and cell lines.

Main Results:

  • Sevoflurane exposure caused spatial memory dysfunction, which mitoQ treatment attenuated.
  • MitoQ modulated mitochondrial dynamics (Mfn1, Mfn2, Drp1, Fis1) and inhibited excessive autophagy (LC3, P62).
  • MitoQ reduced neuroinflammation (NLRP3, ASC) and attenuated apoptosis (Cleaved caspase1, GSDMD).

Conclusions:

  • MitoQ effectively prevents sevoflurane-induced cognitive dysfunction in aged mice.
  • Therapeutic mechanisms involve modulating mitochondrial dynamics, oxidative stress, inflammation, and autophagy.
  • MitoQ shows potential for preventing POCD in elderly patients.