Acetate attenuates perioperative neurocognitive disorders in aged mice
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1Faculty of Anesthesiology, Changhai Hospital, Navy Medical University, Shanghai 200433, China.
Abstract:
Perioperative neurocognitive disorders are common in elderly patients who have undergone surgical procedures. Neuroinflammation induced by microglial activation is a hallmark of these neurological disorders. Acetate can suppress inflammation in the context of inflammatory diseases. We employed an exploratory laparotomy model with isoflurane anesthesia to study the effects of acetate on perioperative neurocognitive disorders in aged mice. Neurocognitive function was assessed with open-field tests and Morris water maze tests 3 or 7 days post-surgery. Acetate ameliorated the surgery-induced cognitive deficits of aged mice and inhibited the activation of IBA-1, a marker of microglial activity. Acetate also reduced expression of inflammatory proteins (tumor necrosis factor-α, interleukin-1β and interleukin-6), oxidative stress factors (NADPH oxidase 2, inducible nitric oxide synthase and reactive oxygen species), and signaling molecules (nuclear factor kappa B and mitogen-activated protein kinase) in the hippocampus. BV2 microglial cells were used to verify the anti-inflammatory effects of acetate in vitro. Acetate suppressed inflammation in lipopolysaccharide-treated BV2 microglial cells, but not when GPR43 was silenced. These results suggest that acetate may bind to GPR43, thereby inhibiting microglial activity, suppressing neuroinflammation, and preventing memory deficits. This makes acetate is a promising therapeutic for surgery-induced neurocognitive disorders and neuroinflammation.
Insights
Acetate helps prevent memory loss after surgery in older mice by reducing brain inflammation. This suggests acetate could be a potential therapy for surgery-induced cognitive decline and neuroinflammation.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Perioperative neurocognitive disorders are common in elderly patients following surgery.
- Microglial activation and subsequent neuroinflammation are key factors in these disorders.
- Acetate demonstrates anti-inflammatory properties in other disease contexts.
Purpose of the Study:
- To investigate the therapeutic potential of acetate in mitigating surgery-induced neurocognitive deficits in aged mice.
- To elucidate the underlying mechanisms of acetate's effects on neuroinflammation and microglial activation.
Main Methods:
- An exploratory laparotomy model with isoflurane anesthesia was used in aged mice.
- Neurocognitive function was assessed using open-field and Morris water maze tests.
- Hippocampal tissue and BV2 microglial cells were analyzed for inflammatory markers and molecular signaling pathways.
Main Results:
- Acetate administration significantly ameliorated cognitive deficits in aged mice post-surgery.
- Acetate inhibited microglial activation (IBA-1) and reduced key inflammatory proteins (TNF-α, IL-1β, IL-6) and oxidative stress markers.
- In vitro studies showed acetate's anti-inflammatory effects in BV2 cells were dependent on GPR43 expression.
Conclusions:
- Acetate effectively prevents surgery-induced cognitive impairment in aged mice by suppressing neuroinflammation.
- The mechanism involves GPR43-mediated inhibition of microglial activation.
- Acetate shows promise as a therapeutic agent for preventing neurocognitive disorders associated with surgery.
