Protective role of dexmedetomidine against sevoflurane-induced postoperative cognitive dysfunction via the

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Wei Wei1, Zhentao Sun1, Shifeng He1

  • 1Department of Anesthesiology, Pain and Perioperative Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, PR China.

Journal of Clinical Neuroscience : Official Journal of the Neurosurgical Society of Australasia
|September 12, 2021
PubMed

Insights

Dexmedetomidine (Dex) protects against postoperative cognitive dysfunction (POCD) by increasing miR-129 levels. This mechanism inhibits TLR4 and NF-κB p65 phosphorylation, improving cognitive function and neuronal health.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Molecular Biology

Background:

  • Postoperative cognitive dysfunction (POCD) is a significant concern.
  • The precise mechanisms underlying Dexmedetomidine's (Dex) role in preventing POCD remain unclear.

Purpose of the Study:

  • To elucidate the mechanism by which Dexmedetomidine (Dex) mitigates sevoflurane-induced postoperative cognitive dysfunction (POCD) in rats.
  • To investigate the role of miR-129 and its downstream targets in Dex's neuroprotective effects.

Main Methods:

  • Rats were exposed to sevoflurane (SEV) to induce POCD, followed by Dexmedetomidine (Dex) treatment.
  • Cognitive and behavioral functions were assessed using the Morris water maze test.
  • Hippocampal and cortical tissues were analyzed for neuronal damage, apoptosis, neuronal activity, microRNA expression, TLR4, and NF-κB p65 phosphorylation.

Main Results:

  • Dexmedetomidine (Dex) treatment alleviated SEV-induced cognitive and behavioral impairments, reduced neuronal apoptosis, and enhanced neuronal activity.
  • Dex administration upregulated miR-129 expression in brain tissues.
  • Inhibition of miR-129 using an antagomir partially reversed Dex's neuroprotective effects.
  • Dex-mediated neuroprotection involved targeting TLR4 and inhibiting NF-κB p65 phosphorylation.

Conclusions:

  • Dexmedetomidine (Dex) ameliorates sevoflurane-induced POCD by upregulating miR-129.
  • The protective mechanism involves the inhibition of the TLR4 and NF-κB p65 signaling pathway.
  • These findings offer potential therapeutic strategies for managing POCD.
Keywords:
DexmedetomidineMicroRNA-129NF-κB p65Postoperative cognitive dysfunctionSevofluraneTLR4

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