Celastrol inhibits pro-inflammatory cytokine secretion in Crohn's disease biopsies.
Crohn's disease is a chronic intestinal inflammatory process. In modern therapy, TNF-alpha inhibition is the main goal. The aim here is to characterize the effects of Celastrol, a pentacyclic-triterpene, on the secretion of inflammatory cytokines by LPS-activated human cells. Celastrol dose-dependently inhibited the secretion of all tested pro-inflammatory cytokines with IC(50) in the nanomolar range. Effect not related to glucocorticoid receptor activity is shown by competition experiments with the steroid antagonist RU486. Celastrol inhibited the pro-inflammatory cytokine secretion from mucosal inflammatory biopsies from Crohn's disease patients. Cytometry emphasized that for all tested pro-inflammatory cytokines, CD33(+) cells are the most sensitive. Quantitative-PCR and confocal analysis on a human monocytic cell line indicated that Celastrol acts at the transcriptional level by inhibiting LPS-induced NF-kappaB translocation. Celastrol might be a putative anti-inflammatory drug in the treatment of inflammatory diseases, given its inhibition of cytokine production by intestinal biopsies from Crohn's disease patients.[1]References
- Celastrol inhibits pro-inflammatory cytokine secretion in Crohn's disease biopsies. Pinna, G.F., Fiorucci, M., Reimund, J.M., Taquet, N., Arondel, Y., Muller, C.D. Biochem. Biophys. Res. Commun. (2004) [Pubmed]
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