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Tag: lipopolysaccharide

Anti-inflammatory effects of ozonated water in an experimental mouse model

This study evaluated the anti-inflammatory effects of ozonated water in a mouse model of acute inflammation induced by lipopolysaccharide (LPS). The results showed that intraperitoneal injection of ozonated water significantly decreased tumor necrosis factor-α (TNF-α) levels and increased superoxide dismutase (SOD) activity, suggesting its potential as an anti-inflammatory agent. Ozonated

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June 26, 2025 No Comments

NLRP3 inflammasome of microglia promotes A1 astrocyte transformation, neo-neuron decline and cognition impairment in endotoxemia

This 2022 in vivo animal study published in Biochemical and Biophysical Research Communications (DOI: 10.1016/j.bbrc.2022.02.092) examined the role of the NLRP3 inflammasome in cognitive decline during endotoxemia. Using a mouse model, researchers found that LPS-induced systemic inflammation elevated IL-1β levels in the cerebrospinal fluid, triggered microglial NLRP3 inflammasome activation, and

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June 26, 2025 No Comments

The endotoxin hypothesis of Alzheimer’s disease

This review introduces the “endotoxin hypothesis” of Alzheimer’s disease (AD), proposing that elevated levels of lipopolysaccharide (LPS)—an endotoxin from Gram-negative bacteria—play a significant role in AD pathogenesis. The article discusses how LPS can enter the bloodstream from gut dysbiosis or infections and accumulate in the brain, promoting amyloid-beta (Aβ) production,

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June 26, 2025 No Comments

The Endotoxin Hypothesis of Parkinson’s Disease

This review explores the “endotoxin hypothesis” of Parkinson’s disease (PD), suggesting that elevated levels of lipopolysaccharide (LPS) from gut dysfunction contribute to PD progression. LPS promotes α-synuclein aggregation, microglial activation, neuroinflammation, and dopaminergic neuron loss in the brain. The hypothesis posits that gut-derived LPS and cytokines induce systemic inflammation, which

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June 26, 2025 No Comments

GluR2 can Drive Neuroinflammation and Cognitive Impairments Following Peripherally Repeated Lipopolysaccharide Exposures

This study demonstrated that GluR2 plays a key role in neuroinflammation and cognitive impairments in a mouse model exposed to repeated peripheral lipopolysaccharide (LPS). LPS exposure led to cognitive deficits, microglial activation, increased GluR1 and GluR2 levels, and reduced synaptic integrity in the hippocampus. The AMPA receptor antagonist CFM-2 and

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June 26, 2025 No Comments

LPS induces microglial activation and GABAergic synaptic deficits in the hippocampus accompanied by prolonged cognitive impairment

This 2023 in vivo animal study published in Scientific Reports (DOI: 10.1038/s41598-023-32798-9) explored how systemic inflammation induced by lipopolysaccharide (LPS) affects microglial activation, synaptic function, and cognition. Using a mouse model, researchers found that microglial activation peaked 3 days after LPS injection and was followed by GABAergic synaptic impairments and

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June 26, 2025 No Comments

Neuroinflammation induced by lipopolysaccharide causes cognitive impairment in mice

This 2019 in vivo study published in Scientific Reports (DOI: 10.1038/s41598-019-42286-8) explored the effects of lipopolysaccharide (LPS)-induced neuroinflammation on cognition in mice. LPS administration activated microglia, increased pro-inflammatory cytokines (TNF-α, IL-1β), decreased anti-inflammatory cytokines (IL-4, IL-10), and impaired memory performance in behavioral tests. It also triggered NF-κB pathway activation and

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June 26, 2025 No Comments

Complement C1q drives microglia-dependent synaptic loss and cognitive impairments in a mouse model of lipopolysaccharide-induced neuroinflammation

This animal study examined the role of complement protein C1q in causing synaptic loss and cognitive impairments through microglial activation in a mouse model of lipopolysaccharide (LPS)-induced neuroinflammation. Researchers found that neutralizing C1q significantly reduced microglial activation, prevented synaptic loss, and protected against cognitive deficits. Clinically, these findings indicate that

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June 26, 2025 No Comments