Abstract
BackgroundNeuroinflammation involves the activation of glial cells in neurodegenerative diseases such as Alzheimer’s disease (AD). Plasmalogens (Pls) are glycerophospholipids constituting cellular membranes and play significant roles in membrane fluidity and cellular processes such as vesicular fusion and signal transduction.MethodsIn this study the preventive effects of Pls on systemic lipopolysaccharide (LPS)-induced neuroinflammation were investigated using immunohistochemistry, real-time PCR methods and analysis of brain glycerophospholipid levels in adult mice.ResultsIntraperitoneal (i.p.) injections of LPS (250 μg/kg) for seven days resulted in increases in the number of Iba-1-positive microglia and glial fibrillary acidic protein (GFAP)-positive astrocytes in the prefrontal cortex (PFC) and hippocampus accompanied by the enhanced expression of IL-1β and TNF-α mRNAs. In addition, β-amyloid (Aβ3–16)-positive neurons appeared in the PFC and hippocampus of LPS-injected animals. The co-administration of Pls (i.p., 20 mg/kg) after daily LPS injections significantly attenuated both the activation of glial cells and the accumulation of Aβ proteins. Finally, the amount of Pls in the PFC and hippocampus decreased following the LPS injections and this reduction was suppressed by co-treatment with Pls.ConclusionsThese findings suggest that Pls have anti-neuroinflammatory and anti-amyloidogenic effects, thereby indicating the preventive or therapeutic application of Pls against AD.
Highlights
Neuroinflammation involves the activation of glial cells in neurodegenerative diseases such as Alzheimer’s disease (AD)
It has been demonstrated in mice and rats that the systemic administration of lipopolysaccharide (LPS) and polyriboinosinic:polyribocytidylic acid, ligands for toll-like receptor (TLR) 4 and TLR 3, respectively, induce neuroinflammation in the central nervous system (CNS), leading to neurodegeneration, the suppression of neurogenesis and the impairment of cognitive behavior [1,2,3]
The present study demonstrated that systemic LPSinduced activation of glial cells, cytokine expression and accumulation of β-amyloid proteins (Aβ) in the prefrontal cortex (PFC) and hippocampus were prevented by co-administration of purified Pls in adult mice
Summary
Neuroinflammation involves the activation of glial cells in neurodegenerative diseases such as Alzheimer’s disease (AD). A single intraperitoneal (i.p.) injection of LPS increases the activity of β-secretase, a Plasmalogens (Pls) are unique glycerophospholipids that contain a vinyl ether bond at the sn-1 position of the glycerol moiety. They are found in all mammalian tissues, especially in the heart and brain, in which ethanolamine Pls (PlsEtn) are much more abundant than choline Pls (PlsCho) [7]. The vinyl ether bond at the sn-1 position makes Pls more susceptible to oxidative stress than corresponding ester bonded glycerophospholipids, which act as antioxidants and protect cells from oxidative stress [10,11,12,13]
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