Title : Kakkalide and its metabolite irisolidone ameliorate carrageenan-induced inflammation in mice by inhibiting NF-κB pathway.

Pub. Date : 2011 Oct

PMID : 20686830






3 Functional Relationships(s)
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1 Kakkalide and irisolidone down-regulated the gene expression of cytokines [tumor necrosis factor alpha (TNF-alpha) and interleukin-1 beta (IL-1beta)] and cyclooxygenase-2 (COX-2) and the production of pro-inflammatory cytokines, TNF-alpha and IL-1beta, and inflammatory mediators, NO and prostaglandin E(2) (PGE(2)), in LPS-stimulated peritoneal macrophages. kakkalide tumor necrosis factor Mus musculus
2 Kakkalide and irisolidone down-regulated the gene expression of cytokines [tumor necrosis factor alpha (TNF-alpha) and interleukin-1 beta (IL-1beta)] and cyclooxygenase-2 (COX-2) and the production of pro-inflammatory cytokines, TNF-alpha and IL-1beta, and inflammatory mediators, NO and prostaglandin E(2) (PGE(2)), in LPS-stimulated peritoneal macrophages. kakkalide tumor necrosis factor Mus musculus
3 Kakkalide and irisolidone down-regulated the gene expression of cytokines [tumor necrosis factor alpha (TNF-alpha) and interleukin-1 beta (IL-1beta)] and cyclooxygenase-2 (COX-2) and the production of pro-inflammatory cytokines, TNF-alpha and IL-1beta, and inflammatory mediators, NO and prostaglandin E(2) (PGE(2)), in LPS-stimulated peritoneal macrophages. kakkalide tumor necrosis factor Mus musculus