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Inflammation is a complex host-protective response against harmful stimuli involving macrophage activation that results in secretion of inflammatory mediators, like nitric oxide (NO), pro-inflammatory cytokines, and prostaglandin E2 (PGE 2 ). In this study, we evaluated fucoidan isolated using Viscozyme-assisted enzymatic extraction of Sargassum coreanum extract against lipopolysaccharide (LPS)-stimulated inflammation in RAW 264.7 macrophages and zebrafish model. Among the fucoidan fractions isolated using ion exchange chromatography, SCVF5 showed the highest sulfate and fucose contents based on chemical composition and monosaccharide analysis. Fourier-transform infrared (FT-IR) spectroscopy confirmed the presence of sulfate esters by the stretching vibrations of the SO peak at 1240 cm -1 . SCVF5 showed anti-inflammatory effects by inhibiting NO and PGE 2 generation in LPS-stimulated RAW 264.7 macrophages by downregulating inducible NO synthase and cyclooxygenase-2 expression. Treatment with SCVF5 suppressed pro-inflammatory cytokine production, such as TNF-α, (IL)-1β, and IL-6 by modulating the nuclear factor-kappa B signaling cascade in LPS-induced RAW 264.7 cells. Furthermore, in vivo results showed that SCVF5 can potentially downregulate LPS-induced toxicity, cell death, and NO production in LPS-induced zebrafish model. Collectively, these results suggest that S. coreanum fucoidan has remarkable anti-inflammatory activity in vitro and in vivo and may have potential applications in the functional food, cosmetic, and pharmaceutical industries., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Inflammation has recently been implicated as a critical mechanism responsible for neurodegenerative diseases. In this study, paeonol (1-(2-hydroxy-4-methoxyphenyl)ethanone) isolated from the sea horse Hippocampus kuda Bleeler was studied as an agent to suppress LPS induced activation of BV-2 microglial and RAW264.7 macrophage cells. The results obtained showed that paeonol significantly suppressed LPS induced release of pro-inflammatory products such as nitric oxide (NO), prostaglandin E2 (PGE(2)), and cytokines; tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). Furthermore, the compound down regulated the protein and gene expression levels of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), TNF-α, IL-1β and IL-6 in both cell lines. Molecular signaling pathway studies showed that paeonol inhibited the translocation of nuclear factor-κB (NF-κB) p65 and p50 subunits to the nucleus by blocking IKKα/β (IκB kinase α/β) mediated degradation of IκBα. Moreover, it suppressed the phosphorylation of mitogen activated protein kinase (MAPK) pathway molecules; c-Jun N-terminal kinases (JNK) and p38 in both cell lines. Collectively these results indicate that paeonol blocked the LPS stimulated inflammatory responses in BV-2 and RAW264.7 cells via modulating MAPK and NF-κB signaling pathways. Therefore, paeonol could be a promising candidate to be used in neuro-inflammatory therapy., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Chitooligosaccharides (COS), the hydrolyzed product of chitosan and its derivatives, are known to have interesting pharmaceutical and medicinal applications due to its high solubility, non-toxicity, and increased functionality. Among them sulfated chitooligosaccharides (SCOSs) have been identified to possess enhanced biological activities. This study reports the effects of SCOSs with different molecular weights on the degradation of articular cartilage through unregulated collagenase expression. The results indicated that the SCOS II (3-5kDa) effectively inhibited the expressions of collagenases 1 and 3 and thereby prevented TNF-α induced degradation of collagen in human chondrosarcoma cells (SW-1353). Moreover, the signaling cascade responsible for this effect was found as SCOS II mediated suppression of NF-κB activation. Based on these data, it can be concluded that SCOS II prevented collagen degradation by inhibiting collagenases 1 and 3 via suppressing TNF-α induced NF-κB signaling. We suggest that SCOS II can be further studied as a potential candidate for the treatment of arthritis., (Crown Copyright © 2012. Published by Elsevier Ltd. All rights reserved.)

Unregulated activation of microglia is a key risk factor contributes to neurodegenerative diseases and suppression of this phenomenon is considered as a potential therapeutic target. The compound isolated from sea horse Hippocampus kuda Bleeler; 1-(5-bromo-2-hydroxy-4-methoxyphenyl)ethanone [SE1] was characterized for its ability in suppressing LPS mediated activation of murine BV-2 cells. Despite the presence of various active molecular groups in the structure, SE1 has not well explored for its biological activities. The outcome of this study clearly indicated that SE1 inhibited the production of inflammatory mediators; nitric oxide, prostaglandin E(2) and pro-inflammatory cytokines. Furthermore, it inhibited the protein and gene expression levels of inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-α, interleukin-1β and interleukin-6. The responsible signaling mechanisms leading to these inhibitions were identified as SE1 mediated blocking of phosphorylation of mitogen activate protein kinase (MAPK) molecules; C-jun-N-terminal kinase (JNK), p38 and nuclear translocation of nuclear factor-κB (NF-κB) p65 and p50 subunits. These results suggest that SE1 has the potential to be further developed as therapeutic against neuro-inflammation., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Ongoing efforts to search for naturally occurring, bioactive substances for the amelioration of arthritis have led to the discovery of natural products with substantial bioactive properties. The seahorse (Hippocampus kuda Bleeler), a telelost fish, is one source of known beneficial products, yet has not been utilized for arthritis research. In the present work, we have purified and characterized a bioactive peptide from seahorse hydrolysis. Among the hydrolysates tested, pronase E-derived hydrolysate exhibited the highest alkaline phosphatase (ALP) activity, a phenotype marker of osteoblast and chondrocyte differentiation. After its separation from the hydrolysate by several purification steps, the peptide responsible for the ALP activity was isolated and its sequence was identified as LEDPFDKDDWDNWK (1821Da). We have shown that the isolated peptide induces differentiation of osteoblastic MG-63 and chondrocytic SW-1353 cells by measuring ALP activity, mineralization and collagen synthesis. Our results indicate that the peptide acts during early to late stages of differentiation in MG-63 and SW-1353 cells. We also assessed the concentration dependence of the peptide's inhibition of MMP (-1, -3 and -13), iNOS and COX-2 expression after treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a common form of phorbol ester. The peptide also inhibited NO production in MG-63 and SW-1353 cells. To elucidate the mechanisms by which the peptide acted, we examined its effects on TPA-induced MAPKs/NF-kappaB activation and determined that the peptide treatment significantly reduced p38 kinase/NF-kappaB in MG-63 cells and MAPKs/NF-kappaB in SW-1353 cells.

Considerable efforts have been taken to identify natural peptides as potential bioactive substances. In this study, novel peptide (SHP-1) derived from seahorse (Hippocampus, Syngnathidae) hydrolysate was explored for its inhibitory effects on collagen release in arthritis with the investigation of its underlying mechanism of action. The efficacy of SHP-1 was determined on cartilage protective effects such as inhibition of collagen and GAG release. SHP-1 was able to suppress not only the expression of collagenases 1 and 3, but also the production of NO via down-regulation of iNOS. However, it presented an irrelevant effect on the level of GAG release in chondrocytic and osteoblastic cells. Inhibition of collagen release by SHP-1 is associated with restraining the phosphorylation of NF-kappaB and p38 kinase cascade. Therefore, it could be suggested that SHP-1 has a potential to be used in arthritis treatment.

Abstract: Two new peptides derived from seaweed pipefish Syngnathus schlegeli, SPP-1(QLGNLGV) and SPP-2 (SVMPVVA) were assessed for their ability to prevent hydrogen peroxide induced oxidative stress in human dermal fibroblasts (HDFs). Both peptides showed a significant hydroxyl radical scavenging activity when tested by ESR technique. And also the peptides effectively suppressed the hydrogen peroxide induced ROS production and DNA damage in HDF cells. Furthermore the two peptides increase the protein expression levels of intracellular antioxidant enzymes SOD1, GSH and catalase in hydrogen peroxide stressed HDF cells. At the cellular signaling level, SPPs block the NF-κB activation which may lead to the reduction of oxidative stress mediated damage of HDF cells. These finding indicate the potential antioxidant effects of SPPs as response to H2O2 stimulation. [Copyright &y& Elsevier]

Fucoidan has been reported to have various biological activities, such as antioxidant, antitumor and anticoagulant, with various health benefits. However, few studies have been conducted to extract fucoidan from Sargassum thunbergii in terms of its immuno-enhancing activities. This aim of this study was to investigate the immuno-enhancing effect of fucoidan (S3) isolated from Sargassum thunbergii through water extraction and ethanol precipitation in RAW 264.7 macrophages and zebrafish. The results showed that S3 contained a relatively high content of fucose and sulfated polysaccharide. Fourier-transform infrared spectroscopy (FTIR) results show that the characteristic peaks at 845 cm−1 and 1220-1270 cm−1 indicate that S3 contains sulfate groups. In vitro , S3 effectively enhanced nitric oxide (NO) production and phagocytic activity. In addition, the results of the study demonstrated that the secretion of tumor necrosis factor-α, interleukin (IL)-6, IL-1β, and IL-10 was upregulated by nuclear factor kappa B (NF-κB) signaling pathway in a dose-dependent manner. In vivo , S3 activates zebrafish immune responses by promoting secretion of NO and activating the NF-κB pathway. Overall, these results suggest that S3 could be used as a functional ingredient added to nutritional supplements and functional foods. • Fucoidan was obtained by water extraction and ethanol precipitation (S3). • S3 activates the NF-ĸB signaling pathway both in vitro and in vivo. • S3 increases macrophage phagocytosis and the levels of immunomodulatory mediators. [ABSTRACT FROM AUTHOR]

Excessive exposure to ultraviolet (UV) irradiation from the sun is the primary environmental factor that causes aging of the skin. Most skin diseases caused by UV are attributed to UVB (280–320 nm). The purpose of this study is to investigate the protective effect of diphlorethohydroxycarmalol (DPHC), isolated from the marine brown alga, Ishige okamurae, against UVB-induced photodamage using both in vitro and in vivo models. Results indicate that DPHC remarkably inhibited commercial collagenase and elastase activities. It also reduced intracellular levels of ROS, improved cell viability and collagen content in UVB-irradiated human dermal fibroblasts (HDF cells). In addition, DPHC significantly inhibited activities of intracellular collagenase and elastase and reduced the expression of matrix metalloproteinases (MMPs) and pro-inflammatory cytokines. These events occurred through regulation of nuclear factor kappa B (NF-κB), activator protein 1 (AP-1), and mitogen-activated protein kinases (MAPKs) signaling pathways in UVB-irradiated HDF cells. Furthermore, DPHC also protected against in vivo photodamage by decreasing cell death through reducing lipid peroxidation and inflammatory response via decreasing ROS levels in UVB-irradiated zebrafish. In conclusion, DPHC has strong in vitro and in vivo photoprotective effects and has the potential to be used as an ingredient in pharmaceutical and cosmeceutical industries. Image 1 • UVB irradiation causes skin aging. • DPHC suppressed UVB-stimulated skin damage in vitro in human dermal fibroblasts. • DPHC suppressed UVB-stimulated skin damage in vivo in zebrafish. • DPHC possesses the potential to be used as an ingredient in pharmaceutical and cosmeceutical industries. [ABSTRACT FROM AUTHOR]