2012
DOI: 10.1186/1742-2094-9-197
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Anti-inflammatory/anti-amyloidogenic effects of plasmalogens in lipopolysaccharide-induced neuroinflammation in adult mice

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 an… Show more

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Cited by 112 publications
(90 citation statements)
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“…Neurons, which are generally not associated with immune functions have been found to play an important role in initiating inflammation and neuron damage. Acute brain injuries, such as stroke, trauma, and hemorrhage, and chronic neurodegenerative diseases including Alzheimer's and Parkinson's diseases are devastating conditions with pathologies that are exacerbated by inflammation and IL-1 [21,23,31]. However, whether neurons under hyperglycemia secrete IL-1β need to be explored.…”
Section: Discussionmentioning
confidence: 98%
“…Neurons, which are generally not associated with immune functions have been found to play an important role in initiating inflammation and neuron damage. Acute brain injuries, such as stroke, trauma, and hemorrhage, and chronic neurodegenerative diseases including Alzheimer's and Parkinson's diseases are devastating conditions with pathologies that are exacerbated by inflammation and IL-1 [21,23,31]. However, whether neurons under hyperglycemia secrete IL-1β need to be explored.…”
Section: Discussionmentioning
confidence: 98%
“…Moreover, unlike the activation of STAT3 and induction of GFAP seen after neurotoxic exposures, suppression of pSTAT3 levels could be achieved with anti-inflammatory pretreatment with CORT. While evidence has been presented suggesting that LPS can over longer times cause neural damage [5], [63]–[66] and accompanying astrogliosis [67][69], our findings here and previously [70], are consistent with an acute and subacute elaboration of cytokines and chemokines as a component of an innate immune response in brain [47], [71]. These neuroinflammatory effects of LPS may reflect a direct action on astrocytes without up regulation of GFAP [43] over acute and subacute times of 2 to 72 hours, or alternatively may reflect an effect on STAT3 in microglia (Fig.…”
Section: Discussionmentioning
confidence: 99%
“…), likely shifting the immunological balance in the proinflammatory direction . Moreover, exogenously applied plasmalogens were reported to prevent serum starvation‐induced neuronal apoptosis in cell culture experiments and to ameliorate systemically induced neuroinflammation in mice, when coadministered intraperitoneally with lipopolysaccharide . Conversely, plasmalogen deficiency may render neurons more vulnerable to stress conditions and inflammation.…”
Section: Molecular Basis and Potential Mechanisms Underlying The Phenmentioning
confidence: 99%