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Remimazolam Attenuates LPS-Derived Cognitive Dysfunction via Subdiaphragmatic Vagus Nerve Target α7nAChR-Mediated

Zhan Zhou1, Ying Yang1, Yi Wei1

  • 1Department of Anesthesiology, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, China.

Neurochemical Research
|March 13, 2024
PubMed

Insights

Remimazolam, an anesthetic, protects against sepsis-induced cognitive dysfunction by reducing neuroinflammation and oxidative stress. It activates the α7nAChR pathway, offering a potential therapeutic target for sepsis-related brain issues.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Immunology

Background:

  • Sepsis-induced neuroinflammation is a major cause of brain dysfunction.
  • Remimazolam is a novel anesthetic with potential organ-protective effects.
  • The impact of remimazolam on sepsis-induced brain impairment remains unclear.

Purpose of the Study:

  • To investigate the protective effects of remimazolam on lipopolysaccharide (LPS)-induced cognitive dysfunction in rats.
  • To elucidate the underlying mechanisms of remimazolam's therapeutic action.

Main Methods:

  • Rats were treated with LPS to induce cognitive impairment.
  • Remimazolam, electroacupuncture (EA), or PNU282987 were administered.
  • Involvement of α7 nicotinic acetylcholine receptor (α7nAChR) and subdiaphragmatic vagus nerve (SDV) was assessed using specific inhibitors (MLA, ML385).
  • Key signaling pathways (Nrf2/HO-1) and protein expressions were analyzed.

Main Results:

  • LPS impaired spatial learning, memory, and cognitive function.
  • Remimazolam treatment ameliorated LPS-induced cognitive dysfunction, splenomegaly, and systemic inflammation.
  • Remimazolam suppressed hippocampal M1 microglial activation and oxidative stress.
  • The protective effects were dependent on α7nAChR activation via the SDV, modulating the Nrf2/HO-1 pathway.
  • Remimazolam upregulated proteins involved in neuroprotection and cognitive function (α7nAChR, Nrf2, HO-1, CREB, BDNF, PSD95).

Conclusions:

  • Remimazolam demonstrates significant neuroprotective effects against LPS-induced brain dysfunction.
  • The mechanism involves the activation of the α7nAChR-mediated Nrf2/HO-1 signaling pathway via the subdiaphragmatic vagus nerve.
  • Remimazolam represents a promising therapeutic agent for sepsis-induced cognitive impairment.
Keywords:
Cognitive dysfunctionLipopolysaccharideMicrogliaNeuroinflammationRemimazolam

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