Abstract
BackgroundGanoderma lucidum (GL) has been widely used in Asian countries for hundreds of years to promote health and longevity. The pharmacological functions of which had been classified, including the activation of innate immune responses, suppression of tumour and modulation of cell proliferations. Effective fractions of Ganoderma lucidum polysaccharides (GLP) had already been reported to regulate the immune system. Nevertheless, the role of GLP in the microglia-mediated neuroinflammation has not been sufficiently elucidated. Further, GLP effect on microglial behavioural modulations in correlation with the inflammatory responses remains to be unravelled. The aim of this work was to quantitatively analyse the contributions of GLP on microglia.MethodsThe BV2 microglia and primary mouse microglia were stimulated by lipopolysaccharides (LPS) and amyloid beta42 (Aβ42) oligomer, respectively. Investigation on the effect of GLP was carried by quantitative determination of the microglial pro- and anti-inflammatory cytokine expressions and behavioural modulations including migration, morphology and phagocytosis. Analysis of microglial morphology and phagocytosis modulations was confirmed in the zebrafish brain.ResultsQuantitative results revealed that GLP down-regulates LPS- or Aβ-induced pro-inflammatory cytokines and promotes anti-inflammatory cytokine expressions in BV-2 and primary microglia. In addition, GLP attenuates inflammation-related microglial migration, morphological alterations and phagocytosis probabilities. We also showed that modulations of microglial behavioural responses were associated with MCP-1 and C1q expressions.ConclusionsOverall, our study provides an insight into the GLP regulation of LPS- and Aβ-induced neuroinflammation and serves an implication that the neuroprotective function of GLP might be achieved through modulation of microglial inflammatory and behavioural responses.
Highlights
Ganoderma lucidum (GL) has been widely used in Asian countries for hundreds of years to promote health and longevity
We showed that Ganoderma lucidum polysaccharides (GLP) inhibited LPS-induced proinflammatory cytokines Interleukin-1 beta (IL-1β), IL-6 and inducible nitric oxide synthase expressions in a concentrationdependent manner (Fig. 1a–c)
The LPS-induced IL-1β and IL-6 expressions were effectively reduced by GLP at 0.1 and 1 μg/ml, and inducible nitric oxide synthase (iNOS) expression down-regulated at 1 μg/ml
Summary
Ganoderma lucidum (GL) has been widely used in Asian countries for hundreds of years to promote health and longevity. The pharmacological functions of which had been classified, including the activation of innate immune responses, suppression of tumour and modulation of cell proliferations. Effective fractions of Ganoderma lucidum polysaccharides (GLP) had already been reported to regulate the immune system. The extract of Ganoderma lucidum (GL) has been isolated [3,4,5] and frequently used in medications as well as in dietary supplements. The effects of GL extracts had been related to the promoted innate immune responses, suppression of cancer cell migration, as well as modulations of cell proliferations [6,7,8]. There have not been sufficient studies in the biochemical mechanism to which GLP might target AD
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