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• W2103247095 abstract "Abstract Background Activated microglial cells have been implicated in a number of neurodegenerative disorders, including Alzheimer's disease (AD), multiple sclerosis (MS), and HIV dementia. It is well known that inflammatory mediators such as nitric oxide (NO), cytokines, and chemokines play an important role in microglial cell-associated neuron cell damage. Our previous studies have shown that CD40 signaling is involved in pathological activation of microglial cells. Many data reveal that cannabinoids mediate suppression of inflammation in vitro and in vivo through stimulation of cannabinoid receptor 2 (CB 2 ). Methods In this study, we investigated the effects of a cannabinoid agonist on CD40 expression and function by cultured microglial cells activated by IFN-γ using RT-PCR, Western immunoblotting, flow cytometry, and anti-CB 2 small interfering RNA (siRNA) analyses. Furthermore, we examined if the stimulation of CB 2 could modulate the capacity of microglial cells to phagocytise Aβ 1–42 peptide using a phagocytosis assay. Results We found that the selective stimulation of cannabinoid receptor CB 2 by JWH-015 suppressed IFN-γ-induced CD40 expression. In addition, this CB 2 agonist markedly inhibited IFN-γ-induced phosphorylation of JAK/STAT1. Further, this stimulation was also able to suppress microglial TNF-α and nitric oxide production induced either by IFN-γ or Aβ peptide challenge in the presence of CD40 ligation. Finally, we showed that CB 2 activation by JWH-015 markedly attenuated CD40-mediated inhibition of microglial phagocytosis of Aβ 1–42 peptide. Taken together, these results provide mechanistic insight into beneficial effects provided by cannabinoid receptor CB 2 modulation in neurodegenerative diseases, particularly AD." @default.
• W2103247095 created "2016-06-24" @default.
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• W2103247095 date "2005-12-01" @default.
• W2103247095 modified "2023-10-16" @default.
• W2103247095 title "Stimulation of cannabinoid receptor 2 (CB2) suppresses microglial activation" @default.
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• W2103247095 doi "https://doi.org/10.1186/1742-2094-2-29" @default.
• W2103247095 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1352348" @default.
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• W2103247095 hasPublicationYear "2005" @default.
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