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Updated: Mar 1, 2026

A Stably Established Two-Point Injection of Lysophosphatidylcholine-Induced Focal Demyelination Model in Mice
Published on: May 11, 2022
[Choline improves lipopolysaccharide-induced central nervous system inflammatory response and cognitive dysfunction
Jun Yu1, Wei-Xing Zhao, Chun-Yan DU
1Department of Anesthesiology and Operation Center, General Hospital of PLA, Beijing 100853, China.E-mail: 18201087627@163.com.
Choline supplementation reduced inflammation and improved cognitive function in mice exposed to lipopolysaccharide (LPS). This neuroprotective effect is mediated by the alpha-7 nicotinic acetylcholine receptor (α7nAChR) pathway, reducing p38 MAPK phosphorylation.
Area of Science:
- Neuroscience
- Pharmacology
- Immunology
Background:
- Lipopolysaccharide (LPS) is a potent endotoxin that triggers neuroinflammation and cognitive deficits.
- Central nervous system (CNS) inflammation is implicated in various neurological disorders.
- Choline, an essential nutrient, plays a role in neurotransmission and neuronal function.
Purpose of the Study:
- To investigate the neuroprotective effects of choline against LPS-induced neuroinflammation and cognitive impairment in mice.
- To elucidate the underlying molecular mechanisms involving the p38 MAPK and α7nAChR signaling pathways.
Main Methods:
- Seventy-two mice were allocated to saline control, LPS, choline intervention, or choline control groups.
- LPS was administered intracerebroventricularly to induce neuroinflammation.
- Choline was administered intraperitoneally prior to LPS injection.
- Locomotor activity, spatial learning, and memory were assessed using the water maze test.
- Hippocampal expressions of Iba1, TNF-α, IL-1β, α7nAChR, p38 MAPK, and phosphorylated p38 MAPK were analyzed.
Main Results:
- LPS administration significantly impaired cognitive function and increased hippocampal inflammatory markers (Iba1, TNF-α, IL-1β) and p38 MAPK phosphorylation.
- Choline pretreatment significantly ameliorated cognitive deficits and reduced levels of Iba1, IL-1β, and phosphorylated p38 MAPK.
- Choline intervention significantly increased the expression of α7nAChR in the hippocampus.
Conclusions:
- Choline exhibits neuroprotective properties against LPS-induced neuroinflammation and cognitive impairment in mice.
- The protective effects of choline are likely mediated through the α7nAChR signaling pathway, inhibiting p38 MAPK phosphorylation.
- Choline represents a potential therapeutic agent for conditions involving neuroinflammation and cognitive dysfunction.
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