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• W2022353036 abstract "An accumulating body of evidence suggests that Alzheimer's disease (AD) is associated with microglia-mediated neuroinflammation and pro-inflammatory cytokine expression. Therefore, the suppression of neuroinflammation and pro-inflammatory cytokine might theoretically slow down the progression of AD. Xanthoceraside, a novel triterpenoid saponin extracted from the husks of Xanthoceras sorbifolia Bunge, has potent antiinflammatory and neuroprotective effects. However, the molecular mechanism underlying its anti-inflammatory action remains unclear. In the present study, we attempted to determine the effects of xanthoceraside on the production of pro-inflammatory mediators in amyloid β25-35 (Aβ25-35)/interferon-γ (IFN-γ)-stimulated microglia. Our results indicated that xanthoceraside (0.01 and 0.1 μM) significantly inhibited the release of nitric oxide (NO) and pro-inflammatory cytokines interleukin-1β and tumor necrosis factor-α in a concentration-dependent manner. Reverse transcriptase-polymerase chain reaction and western blotting analyses showed that xanthoceraside decreased the Aβ25-35/IFN-γ-induced production of cyclooxygenase-2 and inducible NO synthase. These effects were accompanied by inhibited activities of nuclear factor-κB and mitogen-activated protein kinase through Toll-like receptor 2 in a myeloid differentiation protein 88-dependent manner. Our results provide support for the therapeutic potential of xanthoceraside in AD." @default.
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• W2022353036 date "2013-01-01" @default.
• W2022353036 modified "2023-10-17" @default.
• W2022353036 title "Xanthoceraside Inhibits Pro-inflammatory Cytokine Expression in Aβ25–35/IFN-γ–Stimulated Microglia Through the TLR2 Receptor, MyD88, Nuclear Factor-κB, and Mitogen-Activated Protein Kinase Signaling Pathways" @default.
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• W2022353036 doi "https://doi.org/10.1254/jphs.13031fp" @default.
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