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Brown algae are known to contain rich anti-inflammatory compounds. The objective of this study was to identify anti-inflammatory compound in the Sargassum macrocarpum and anti-inflammatory effect of tuberatolide B (TTB) was investigated. TTB significantly suppressed the production of NO and pro-inflammatory cytokines such as interleukin (IL)-6 and IL-1β. In addition, the mechanism involved in the inhibition of the inflammatory effect of LPS by TTB was investigated. The results showed that TTB aforementioned this effect through NF-κB and MAPKs phosphorylation pathways. We also assessed the anti-inflammatory activity of TTB using in vivo zebrafish model. In LPS-stimulated zebrafish, TTB enhanced survival and significantly inhibited the NO production and mRNA expression of inducible NO synthase. Therefore, anti-inflammatory activity of TTB against LPS in RAW264.7 cells and the zebrafish model was determined. These finding suggest that TTB may be used as functional anti-inflammatory foods and nutraceuticals.

Graphical abstract Highlights • TTB is an effective anti-inflammatory agent to develop nutraceutical. • TTB suppresses NO production through inhibition of MAPKs/ NF-κB phosphorylation. • In zebrafish, TTB significantly reduced the production of NO and expression of iNOS. Abstract Brown algae are known to contain rich anti-inflammatory compounds. The objective of this study was to identify anti-inflammatory compound in the Sargassum macrocarpum and anti-inflammatory effect of tuberatolide B (TTB) was investigated. TTB significantly suppressed the production of NO and pro-inflammatory cytokines such as interleukin (IL)-6 and IL-1β. In addition, the mechanism involved in the inhibition of the inflammatory effect of LPS by TTB was investigated. The results showed that TTB aforementioned this effect through NF-κB and MAPKs phosphorylation pathways. We also assessed the anti-inflammatory activity of TTB using in vivo zebrafish model. In LPS-stimulated zebrafish, TTB enhanced survival and significantly inhibited the NO production and mRNA expression of inducible NO synthase. Therefore, anti-inflammatory activity of TTB against LPS in RAW264.7 cells and the zebrafish model was determined. These finding suggest that TTB may be used as functional anti-inflammatory foods and nutraceuticals. [ABSTRACT FROM AUTHOR]

Tuberatolide B (TTB, C27H34O4) is a diastereomeric meroterpenoid isolated from the Koreanmarine algae Sargassum macrocarpum. However, the anticancer effects of TTB remain unknown. In this study, we demonstrate that TTB inhibits tumor growth in breast, lung, colon, prostate, and cervical cancer cells. To examine themechanismby which TTB suppresses cell growth, we determined the effect of TTB on apoptosis, ROS generation, DNA damage, and signal transduction. TTB induced ROS production in MDA-MB-231, A549, and HCT116 cells. Moreover, TTB enhanced DNA damage by inducing γH2AX foci formation and the phosphorylation of DNA damage-related proteins such as Chk2 and H2AX. Furthermore, TTB selectively inhibited STAT3 activation, which resulted in a reduction in cyclin D1, MMP-9, survivin, VEGF, and IL-6. In addition, TTB-induced ROS generation caused STAT3 inhibition, DNA damage, and apoptotic cell death. Therefore, TTB suppresses cancer progression by promoting ROS-mediated inhibition of STAT3 signaling, suggesting that TTB is useful for the treatment of cancer. [ABSTRACT FROM AUTHOR]

Tuberatolide B (TTB, C 27 H 34 O₄) is a diastereomeric meroterpenoid isolated from the Korean marine algae Sargassum macrocarpum . However, the anticancer effects of TTB remain unknown. In this study, we demonstrate that TTB inhibits tumor growth in breast, lung, colon, prostate, and cervical cancer cells. To examine the mechanism by which TTB suppresses cell growth, we determined the effect of TTB on apoptosis, ROS generation, DNA damage, and signal transduction. TTB induced ROS production in MDA-MB-231, A549, and HCT116 cells. Moreover, TTB enhanced DNA damage by inducing γH2AX foci formation and the phosphorylation of DNA damage-related proteins such as Chk2 and H2AX. Furthermore, TTB selectively inhibited STAT3 activation, which resulted in a reduction in cyclin D1, MMP-9, survivin, VEGF, and IL-6. In addition, TTB-induced ROS generation caused STAT3 inhibition, DNA damage, and apoptotic cell death. Therefore, TTB suppresses cancer progression by promoting ROS-mediated inhibition of STAT3 signaling, suggesting that TTB is useful for the treatment of cancer.