期刊
JOURNAL OF PHARMACOLOGICAL SCIENCES
卷 129, 期 2, 页码 101-106出版社
JAPANESE PHARMACOLOGICAL SOC
DOI: 10.1016/j.jphs.2015.05.003
关键词
Fumigaclavine C; Colitis; NLRP3 inflammasome; IL-1 beta; Caspase-1
资金
- Natural Science Foundation of China [81402938, 81422050]
- Natural Science Foundation of Jiangsu Province [BK2014575]
In the present study, the effect of Fumigaclavine C, a fungal metabolite, on murine experimental colitis induced by dextran sulfate sodium (DSS) and its possible mechanism were examined in vivo and vitro. Oral administration of Fumigaclavine C dose-dependently attenuated the loss of body weight and shortening of colon length induced by DSS. The disease activity index, histopathologic scores of musco was also significantly reduced by Fumigaclavine C treatment. Protein and mRNA levels of DSS-induced pro-inflammatory cytokines in colon, including TNF-alpha, IL-1 beta and IL-17A, were markedly suppressed by Fumigaclavine C. At the same time, decreased activation of caspase-1 in peritoneal macrophages was detected in Fumigaclavine C -treated mice which suggested that the NLRP3 inflammasome activation was suppressed. Furthermore, in the LPS plus ATP cell model, we found that Fumigaclavine C dose-dependent inhibited IL-1 beta release and caspase-1 activation. Taken together, our results demonstrate the ability of Fumigaclavine C to inhibit NLRP3 inflammasome activation and give some evidence for its potential use in the treatment of inflammatory bowel diseases. (C) 2015 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society.
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