Inhibition of NFκB-mediated inflammatory response by β-damascenone

The transcription factor NFκB is one of the central regulators within the immune system. It is activated by various stimuli like cytokines and bacterial products. NFκB controls over 150 target genes, including genes regulating immune response and inflammation [1]. Recently we have found that an active component of Epipremnum pinnatum, β-damascenone, was able to inhibit the induction of NFκB-dependent genes in human endothelial and monocyte-like cells stimulated by bacterial lipopolysaccharide (LPS) that activates the NFκB signalling pathway via the Toll-like receptor 4 (TLR4) [2].

The goal of the present work was to examine whether β-damascenone can also inhibit the cellular response to the proinflammatory cytokines TNF-α and IL-1β, which stimulate cells via cytokine receptors. β-Damascenone inhibited E-selectin mRNA expression in HUVECtert cells and TNF-α gene expression in THP-1 cells stimulated by either IL-1β or TNFα. We conclude that β-damascenone acts at the post-receptor level, most likely via inhibiting the NFκB signalling pathway, which is shared by all three receptors. Further investigations to confirm this mechanism are in progress.

Fig. 1 Structure of β-damascenone

• References

• 1 Pahl HL. Activators and target genes of Rel/NF-κB transcription factors. Oncogene 1999; 18: 6853 EP . DOI:10.1038/sj.onc.1203239
• 2 Hayden MS, Ghosh S. NF-κB, the first quarter-century: remarkable progress and outstanding questions. Genes Dev 2012; 26 203–234. DOI: 10.1101/gad.183434.111.