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Dexmedetomidine improves postoperative cognitive dysfunction via regulating Adrb2/Pkg: Dexmedetomidine against

Cuirong Chen1, Hong Han2, Hongzhe Li3

  • 1Department of Anesthesiology, Tianjin Cancer Hospital Airport Hospital, Tianjin 300308, China.

Neuroscience Letters
|October 3, 2025
PubMed
Summary

Dexmedetomidine (Dex) protects rats against postoperative cognitive dysfunction (POCD) by upregulating Adrb2 and Pkg. This mechanism involves alleviating inflammation and suppressing apoptosis, improving cognitive function.

Keywords:
Adrb2BV-2DexmedetomidinePkgPostoperative cognitive dysfunction

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Molecular Biology

Background:

  • Postoperative cognitive dysfunction (POCD) presents as neurological complications affecting daily life.
  • Understanding the mechanisms behind POCD is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of Adrb2 and Pkg in the protective effects of Dexmedetomidine (Dex) against POCD in a rat model.
  • To elucidate the molecular targets of Dex in mitigating cognitive impairment.

Main Methods:

  • Constructed a POCD rat model and assessed cognitive function using Morris water maze tests.
  • Measured inflammatory markers (IL-6, TNF-α, IL-13) and Adrb2/Pkg mRNA levels in hippocampus tissue.
  • Utilized LPS-induced BV-2 cells to verify the role of Adrb2/Pkg.

Main Results:

  • Network pharmacology identified Adrb2 and Pkg as key targets for Dex in POCD.
  • Dex improved learning and memory in POCD rats, reduced inflammation, and increased Adrb2/Pkg expression.
  • Silencing Adrb2/Pkg reversed Dex-mediated suppression of apoptosis in inflammatory cells.

Conclusions:

  • The Adrb2/Pkg pathway is a potential mechanism for Dex-induced protection against POCD.
  • Dexmedetomidine demonstrates therapeutic potential for preventing and treating postoperative cognitive dysfunction.