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Published on: June 2, 2015
Esketamine improves cognitive function in sepsis-associated encephalopathy by inhibiting microglia-mediated
1College of Anesthesia, Guizhou Medical University, Guizhou Province, Guiyang 550004, China; Department of Anesthesiology, The Affiliated Hospital of Guizhou Medical University, Guizhou Province, Guiyang 550004, China; Guizhou Medical University Key Laboratory of Anesthesia and Pain Mechanism Research, Guizhou Province, Guiyang, 550004, China.
Abstract:
Microglia-mediated neuroinflammation is critical in the pathogenesis of sepsis-associated encephalopathy(SAE). Identifying the key factors that inhibit microglia-mediated neuroinflammation holds promise as a potential target for preventing and treating SAE. Esketamine, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, has been proposed to possess protective and therapeutic properties against neuroinflammatory disorders. This study provides evidence that the administration of Esketamine in SAE mice improves cognitive impairments and alleviates neuronal damage by inhibiting the microglia-mediated neuroinflammation. The BDNF receptor antagonist K252a was employed in both vivo and in vitro experiments. The findings indicate that K252a successfully counteracted the beneficial effects of Esketamine on microglia and cognitive behavior in mice with SAE. Consequently, these results suggest that Esketamine inhibits microglia-mediated neuroinflammation by activating the BDNF pathway, and mitigating neuronal damage and cognitive dysfunction associated with SAE.
Insights
Esketamine administration in sepsis-associated encephalopathy (SAE) mice improves cognition and reduces neuronal damage by inhibiting neuroinflammation. This effect is mediated by activating the brain-derived neurotrophic factor (BDNF) pathway.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Microglia-mediated neuroinflammation is a key factor in sepsis-associated encephalopathy (SAE).
- Targeting neuroinflammation offers potential therapeutic strategies for SAE.
Purpose of the Study:
- To investigate the efficacy of esketamine in mitigating SAE.
- To elucidate the role of the brain-derived neurotrophic factor (BDNF) pathway in esketamine's neuroprotective effects.
Main Methods:
- Administration of esketamine to SAE mice.
- In vivo and in vitro experiments using the BDNF receptor antagonist K252a.
- Assessment of cognitive function and neuronal damage.
Main Results:
- Esketamine improved cognitive impairments and alleviated neuronal damage in SAE mice.
- K252a counteracted the beneficial effects of esketamine, indicating pathway involvement.
- Esketamine inhibited microglia-mediated neuroinflammation.
Conclusions:
- Esketamine exerts neuroprotective effects in SAE by inhibiting microglia-mediated neuroinflammation.
- The brain-derived neurotrophic factor (BDNF) pathway is crucial for esketamine's therapeutic actions in SAE.
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