Bo-Ram Ye

Photo-oxidative stress by ultraviolet-B radiation and antioxidative defense of eckstolonol in human keratinocytes

Ultraviolet-B (UV-B) irradiation has been known to generate oxidative stress by increasing reactive oxygen species (ROS) in skin cells. Several naturally occurring antioxidant compounds isolated from marine algae are believed to protect against ROS. In this study, we assessed the antioxidative effect of eckstolonol isolated from Ecklonia cava against UV-B-induced ROS in human keratinocytes (HaCaTs). We investigated the effects of photo-oxidative stress by UV-B (50 mJ/cm(2)) and the antioxidative effects of eckstolonol using fluorometry, flow cytometry, microscopy, and cell viability and comet assays. UV-B irradiation decreased cell viability, which was restored in a dose-dependent manner with eckstolonol treatment (0, 5, 50, 100, and 200 μM). Moreover, eckstolonol reduced UV-B-induced ROS, lipid peroxidation, damaged DNA levels, and cell death. These antioxidative effects seem to be due to the enzymatic activities of catalase (CAT) and superoxide dismutase (SOD). Collectively, these results indicate that eckstolonol is capable of protecting keratinocytes from photo-oxidative stress.

Chromene suppresses the activation of inflammatory mediators in lipopolysaccharide-stimulated RAW 264.7 cells

Inflammation is complex process involving a variety of immune cells that defend the body from harmful stimuli. However, pro-inflammatory cytokines and inflammatory mediators can also exacerbate diseases such as cancer. The aim of this study was to identify a natural effective remedy for inflammation. We isolated a functional algal chromene compound from Sargassum siliquastrum, named sargachromanol D (SD). We evaluated the anti-inflammatory effect of SD on lipopolysaccharide (LPS)-exposed RAW 264.7 cells by measuring cell viability, cytotoxicity, and production of inflammatory mediators such as nitric oxide (NO), prostaglandin E2 (PGE2), inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and the pro-inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6. SD inhibited production of NO and PGE2 from LPS-induced cells by preventing the expression of inflammatory mediators such as iNOS and COX-2 in a dose-dependent manner. Concurrently, levels of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 were reduced with increasing concentrations of SD. In addition, SD inhibited the activation of NF-κB and mitogen-activated protein kinases (MAPKs) pathways in a concentration-dependent manner. These results indicate that SD inhibits LPS-stimulated inflammation by inhibition of the NF-κB and MAPKs pathways in macrophages.

Draft Genome Sequence of Marinobacterium stanieri S30, a Strain Isolated from a Coastal Lagoon in Chuuk State in Micronesia

In this study, we isolated xylan-degrading bacteria from a coastal lagoon of Micronesia and identified the bacteria as Marinobacterium stanieri S30. GSFLX 454 pyrosequencing and sequence analysis of the M. stanieri S30 genome generated 4,007 predicted open reading frames (ORFs) that could be candidate genes for producing enzymes with different catalytic functions.

Tuberatolide B Suppresses Cancer Progression by Promoting ROS-Mediated Inhibition of STAT3 Signaling

Tuberatolide B (TTB, C27H34O4) 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.

Induction of apoptosis by the tropical seaweed Pylaiella littoralis in HT-29 cells via the mitochondrial and MAPK pathways

We demonstrated that an extract from Pylaiella littoralis, collected from the Federate States of Micronesia (FSM), could inhibit the proliferation of tumor cells. P. littoralis extract (PLE) showed anti-proliferative activities in the tumorigenic cells tested, ranging from 20.2% to 67.9%. The highest inhibitory activity, in HT-29 cells, was selected for further experiments. PLE showed no cytotoxic effect in normal cells and inhibited the growth of HT-29 cells depending on concentration and incubation time. PLE-treated HT-29 cells showed the typical morphological characteristics of apoptosis, such as apoptotic body formation and DNA fragmentation. PLE also induced mitochondrial membrane potential depolarization and resulted in increased mitochondrial membrane permeability, compared with untreated cells. PLE decreased Bcl-2 protein and increased Bax protein expression, activating caspase-3 and poly (ADP-ribose) polymerase (PARP) expression via the caspase pathway. PLE also increased the phosphorylation of c-Jun N-terminal kinase (JNK), p38, and extracellular signal-regulated kinase (ERK), and it reduced cell viability in treatment cells with specific inhibitors such as PD98059 (a specific inhibitor of ERK), SP600125 (a specific inbibitor of JNK), and SB 203580 (a specific inbibitor of p38 MAPK). via the the mitogen-activated protein kinases (MAPKs) pathway. These results suggest that PLE inhibits the proliferation of HT-29 cells by affecting the caspase and MAPK pathways involved in the induction of apoptosis. Thus, we suggest that P. littoralis extract might be potential candidate agents for the treatment of human colorectal cancer.

Draft Genome Sequence of the Xylan-Degrading Marine Bacterium Strain S124, Representing a Novel Species of the Genus Oceanicola

We isolated a xylan-degrading bacterium from seawater of Micronesia and identified it as Oceanicola sp. strain S124. We sequenced the Oceanicola sp. S124 genome using GSFLX 454 pyrosequencing and predicted 4,433 open reading frames (ORFs) including putative saccharification and phage-related genes.

Anti-inflammatory effect of Apo-9′-fucoxanthinone via inhibition of MAPKs and NF-kB signaling pathway in LPS-stimulated RAW 264.7 macrophages and zebrafish model

ABSTRACT In this study, we confirmed the anti‐inflammatory effect of Apo‐9‐fucoxanthinone (AF) in in vitro RAW 264.7 cells and in vivo zebrafish model. In lipopolysaccharide (LPS)‐stimulated zebrafish, AF significantly decreased the production of reactive oxygen species (ROS), nitric oxide (NO) and cell death. In addition, the mRNA expression of inducible nitric oxide synthase (iNOS), suppressed cyclooxygenase‐2 (COX‐2) and an inflammatory cytokines; IL‐1&bgr;, TNF‐&agr; were shown reduction. And AF significantly inhibited NO production and expression of iNOS in LPS‐stimulated RAW 264.7 cells. Further, AF suppressed COX‐2, prostaglandin E2 (PGE2), and pro‐inflammatory cytokines such as interleukin‐6 (IL‐6), IL‐1&bgr;, and tumor necrosis factor‐&agr; (TNF‐&agr;) at 25, 50 and 100&mgr;g/mL, respectively. Further mechanistic studies showed that AF suppressed the nuclear factor‐kB (NF‐kB) pathway and phosphorylation of mitogen‐activated protein kinase (MAPK) pathway molecules such as extracellular signal‐regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK). According to the results, AF can be used and applied as a useful anti‐inflammatory agent of nutraceutical or pharmaceutical. HIGHLIGHTSAnti‐inflammatory effect of Apo‐9‐fucoxanthinone in in vitro RAW 264.7 cells and in vivo zebrafishApo‐9‐fucoxanthinone suppressed NO production through NF‐kB and MAPKs pathway.In LPS‐stimulated zebrafish, Apo‐9‐fucoxanthinone significantly decreased ROS, NO, cell death and pro‐inflammatory cytokines.Apo‐9‐fucoxanthinone can be extremely useful as an effective anti‐inflammatory agent.

Bis (3-bromo-4,5-dihydroxybenzyl) ether, a novel bromophenol from the marine red alga Polysiphonia morrowii that suppresses LPS-induced inflammatory response by inhibiting ROS-mediated ERK signaling pathway in RAW 264.7 macrophages

Inflammation is a pathophysiological defense response against various factors for maintaining homeostasis in the body. However, when continued excessive inflammation becomes chronic, various chronic diseases can develop. Therefore, effective treatment before chronic inflammation development is essential. Bis (3-bromo-4,5-dihydroxybenzyl) ether (BBDE, C14H12Br2O5) is a novel bromophenol isolated from the red alga Polysiphonia morrowii. The beneficial physiological functions of various bromophenols are known, but whether BBDE has beneficial physiological functions is unknown. Therefore, we first investigated whether BBDE exerts any anti-inflammatory effect. We demonstrated that BBDE inhibits inflammation by reducing inflammatory mediators, such as nitric oxide, prostaglandin E2, iNOS, COX2, and pro-inflammatory cytokines (tumor necrosis factor-α, interleukin-1β, and interleukin-6), in LPS-induced macrophage cells. To examine the mechanism of action by which BBDE inhibits inflammation, we confirmed its effect on signal transduction and ROS generation. BBDE selectively inhibited ERK phosphorylation in the mitogen-activated protein kinase pathways. Moreover BBDE suppressed LPS-induced ROS generation in RAW 264.7 macrophage cells. Inhibition of LPS-induced ROS generation by BBDE also caused ERK inactivation and an inflammatory reaction. Therefore, BBDE inhibits LPS-induced inflammation by inhibiting the ROS-mediated ERK signaling pathway in RAW 264.7 macrophage cells and thus can be useful for treating inflammatory diseases.