Fucoxanthin from microalgae Phaeodactylum tricornutum inhibits pro-inflammatory cytokines by regulating both NF-kB and NLRP3 inflammasome activation
- Fucoxanthin from microalgae Phaeodactylum tricornutum inhibits pro-inflammatory cytokines by regulating both NF-kB and NLRP3 inflammasome activation
- 구송이; 김상민; 이아현; 신혜윤; 박종휘; 양승훈
- fucoxanthin; Pheodactylum; NF-kB; cytokines
- Issue Date
- Scientific Reports
- VOL 11-555
- Pro-infammatory cytokines such as IL-1β, IL-6, and TNF-α are mediated by the activation of various kinds of signaling pathways in the innate immune system. Particularly, NF-κB and NLRP3 infammasome signaling are involved in the production and secretion of these cytokines. Each signaling is participated in the two steps necessary for IL-1β, a representative pro-infammatory cytokine, to be processed into a form secreted by cells. In the priming step stimulated by LPS, pro-IL-1β is synthesized through NF-κB activation. Pro-IL-1β cleavages into mature IL-1β by formed NLRP3 infammasome in the activation step induced by ATP. The mature form of IL-1β is subsequently secreted out of the cell, causing infammation. Moreover, IL-6 and TNF-α are known to increase in NLRP3 infammasome-mediated conditions. Here, we found that fucoxanthin, one of the major components of Phaeodactylum tricornutum, has an inhibitory efect on NF-κB and NLRP3 infammasome activation induced by the combination of LPS and ATP in bone marrowderived immune cells as well as astrocytes. Fucoxanthin, which is abundant in the EtOH fraction of Phaeodactylum tricornutum extracts, has shown to have less cell toxicity and found to decrease the production of major pro-infammatory cytokines such as IL-1β, IL-6, and TNF-α. Fucoxanthin has also shown to suppress the expression of cleaved caspase-1 and the oligomerization of ASC, which are the main components of the NLRP3 infammasome. Furthermore, phosphorylated IκBα and pro-IL-1β expression decreased in the presence of fucoxanthin, suggesting that fucoxanthin can negatively regulate the priming step of infammasome signaling. Thus, our results provide reliable evidence that fucoxanthin may serve as a key candidate in the development of potential therapeutic agents for infammatory diseases as well as neurodegenerative diseases caused by NF-κB and NLRP3 infammasome activation.
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