Bromophenol (5-bromo-3,4-dihydroxybenzaldehyde) isolated from red alga Polysiphonia morrowii inhibits adipogenesis by regulating expression of adipogenic transcription factors and AMP-activated protein kinase activation in 3T3-L1 adipocytes.

The aim of the present study was to investigate the effect of 5-bromo-3,4-dihydroxybenzaldehyde (BD) isolated from Polysiphonia morrowii on adipogenesis and differentiation of 3T3-L1 preadipocytes into mature adipocytes and its possible mechanism of action. Levels of lipid accumulation and triglyceride were significantly lower in BD treated cells than those in untreated cells. In addition, BD treatment reduced protein expression levels of peroxisome proliferator-activated receptor-γ, CCAAT/enhancer-binding proteins α, and sterol regulatory element-binding protein 1 compared with control (no treatment). It also reduced expression levels of adiponectin, leptin, fatty acid synthase, and fatty acid binding protein 4. AMP-activated protein kinase activation was found to be one specific mechanism involved in the effect of BD. These results demonstrate that BD possesses inhibitory effect on adipogenesis through activating AMP-activated protein kinase signal pathway.

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-1ß, 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.

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.

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-1ß, TNF-α 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-1ß, and tumor necrosis factor-α (TNF-α) at 25, 50 and 100 µg/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.

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.

5-Bromo-2-hydroxy-4-methyl-benzaldehyde inhibited LPS-induced production of pro-inflammatory mediators through the inactivation of ERK, p38, and NF-κB pathways in RAW 264.7 macrophages.

The aim of the present study was to investigate the effects of 5-bromo-2-hydroxy-4-methyl-benzaldehyde (BHMB) on inflammatory responses to lipopolysaccharide (LPS) in RAW 264.7 cells and the associated mechanism of action. BHMB concentration-dependently suppressed protein and mRNA expressions of iNOS and COX-2, thereby inhibiting the production of NO and PGE2 in LPS-stimulated RAW 264.7 cells. BHMB also reduced the mRNA expression of TNF-α, IL-6, and IL-1ß in LPS-stimulated RAW 264.7 cells. To elucidate the mechanism underlying the anti-inflammatory activity of BHMB, we investigated the effects of BHMB on the mitogen-activated protein kinase and nuclear factor-kappa B (NF-κB) pathways. BHMB suppressed the phosphorylation and degradation of IκB-α and markedly inhibited the nuclear translocation of p65 and p50 in LPS-stimulated RAW 264.7 cells. The compound also inhibited the LPS-stimulated phosphorylation of ERK and p38. Taken together, these results illustrated that BHMB suppresses pro-inflammatory mediator and cytokine expression in LPS-stimulated RAW 264.7 cells by inhibiting the phosphorylation of ERK and p38 and the activation of NF-κB.

Ochrovirga pacifica gen. nov., sp. nov., a novel agar-lytic marine bacterium of the family Flavobacteriaceae isolated from a seaweed.

A strain designated as S85(T) was isolated from a seaweed collected from coastal area of Chuuk State in Micronesia. The strain was gram-negative, rod-shaped, and non-motile and formed yellow colonies on the SWY agar (0.2 % yeast extract and 1.5 % agar in seawater) and Marine agar 2216. The strain grew at pH 5-9 (optimum, pH 8), at 15-40 °C (optimum, 25-28 °C), and with 1-9 % (w/v) NaCl (optimum, 3 %). The phylogenetic analysis based on 16S rRNA gene sequence showed that strain S85(T) was related to Lutibacter litoralis CL-TF09(T) and Maritimimonas rapanae A31(T) with 91.4 % and with 90.5 % similarity, respectively. The dominant fatty acids were iso-C15:0, iso-C15:0 3-OH and iso-C17:0 3-OH, C16:0 3-OH and summed feature 3 (C16:1 ω7c and/or iso-C15:0 2-OH). The major isoprenoid quinone was MK-6. The DNA G+C content of the type strain was 34.6 mol %. The major polar lipids were phosphatidylethanolamine, an unknown glycolipid and two unknown polar lipids. Based on this polyphasic taxonomic data, strain S85(T) stands for a novel species of a new genus, and we propose the name Ochrovirga pacifica gen. nov., sp. nov. The type strain of O. pacifica is S85(T) (=KCCM 90106 =JCM 18327(T)).

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)-1ß, 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-1ß, 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 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.

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.

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.