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• W2013221532 abstract "Regulation of signal transducer and activator of transcription (STAT) 1 signaling is being explored as a new approach to the treatment of inflammatory bowel diseases. However, few chemicals have been reported to inhibit IFN-γ/STAT1 signaling for Crohn's disease therapy. In the present study, we found that cirsilineol, a small natural compound isolated from Artemisia vestita, significantly ameliorated trinitro-benzene sulfonic acid (TNBS)-induced T-cell-mediated experimental colitis in mice, which was closely associated with reduced autoreactive T-cell proliferation and activation. Moreover, the regulatory action of pro-inflammatory and anti-inflammatory cytokine by cirsilineol treatment was found to decrease the activity of effector Th1 cells but increase the activity of regulatory T cells as characterized by down-regulation of IFN-γ and corresponding up-regulation of IL-10 and TGF-β. The therapeutic effect of cirsilineol was attributable to a novel regulatory mechanism with selective inhibiting IFN-γ signaling in colonic lamina propria CD4+ T cells, which was mediated through down-regulating STAT1 activation and T-bet expression. Furthermore, cirsilineol was found to down-regulate the activation of JAK2, a critical kinase for IFN-γ/STAT1 signaling, and abrogate the expression of T-bet, resulting in markedly decreased proliferation and activation of T cells in vitro. Importantly, the inhibition of IFN-γ/STAT1 signaling by cirsilineol was reversible in the presence of high level of IFN-γ. These results strongly suggest that cirsilineol might be potentially useful for treating T-cell-mediated human inflammatory bowel diseases." @default.
• W2013221532 created "2016-06-24" @default.
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• W2013221532 date "2010-01-01" @default.
• W2013221532 modified "2023-10-16" @default.
• W2013221532 title "Novel immunomodulatory properties of cirsilineol through selective inhibition of IFN-γ signaling in a murine model of inflammatory bowel disease" @default.
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• W2013221532 doi "https://doi.org/10.1016/j.bcp.2009.08.014" @default.
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