Bok-Mi Jung

Protective effects against H2O2-induced damage by enzymatic hydrolysates of an edible brown seaweed, sea tangle (Laminaria japonica).

Enzymatic hydrolysates of Laminaria japonica were evaluated for antioxidative activities using hydroxyl radical scavenging activity and protective effects against H(2)O(2)-induced DNA and cell damage. In addition, activities of antioxidative enzymes, including catalase, glutathione peroxidase, and glutathione S-transferase, of the enzymatic hydrolysates from L. japonica were also estimated. L. japonica was first enzymatically hydrolyzed by seven carbohydrases (Dextrozyme, AMG, Promozyme, Maltogenase, Termamyl, Viscozyme, and Celluclast [all from Novo Co., Novozyme Nordisk, Bagsvaerd, Denmark]) and five proteinases (Flavourzyme, Neutrase, Protamex, Alcalase [all from Novo Co.], and pancreatic trypsin). The hydroxyl radical scavenging activities of Promozyme and pancreatic trypsin hydrolysates from L. japonica were the highest as compared to those of the other carbohydrases and proteinases, and their 50% inhibitory concentration values were 1.67 and 317.49 mug/mL, respectively. The pancreatic trypsin hydrolysates of L. japonica exerted a protective effect on H(2)O(2)-induced DNA damage. We also evaluated the protective effect on hydroxyl radical-induced oxidative damage in PC12 cells via propidium iodide staining using a flow cytometer. The AMG and pancreatic trypsin hydrolysates of L. japonica dose-dependently protected PC12 cells against cell death caused by hydroxyl radical-induced oxidative damage. Additionally, we analyzed the activity of antioxidative enzymes such as catalase, glutathione peroxidase, and the phase II biotransformation enzyme glutathione S-transferase in L. japonica-treated cells. The activity of all antioxidative enzymes was higher in L. japonica-treated cells compared with the nontreated cells. These results indicate that enzymatic hydrolysates of L. japonica possess antioxidative activity.

Anti-inflammatory effect of ethanolic extract from Myagropsis myagroides on murine macrophages and mouse ear edema

BackgroundThis study aims to investigate anti-inflammatory effect of ethanolic extract of Myagropsis myagroides (EMM) in the lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and the phorbol 12-myristate 13-acetate (PMA)-induced ear edema in mice, and to clarify its underlying molecular mechanisms.MethodsThe levels of nitric oxide (NO), prostaglandin E2 (PGE2), and pro-inflammatory cytokines were measured by Griess assay and enzyme linked immunosorbent assay. The expressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), mitogen-activated protein kinases (MAPKs), and Akt were measured using Western blotting. Nuclear translocation and transcriptional activation of nuclear factor-κB (NF-κB) were determined by immunocytochemistry and reporter gene assay, respectively. PMA-induced mouse ear edema was used as the animal model of inflammation. Anti-inflammatory compounds in EMM were isolated using high-performance liquid chromatography and identified by nuclear magnetic resonance.ResultsEMM significantly inhibited the production of NO, PGE2, and pro-inflammatory cytokines in a dose-dependent manner and suppressed the expression of iNOS and COX-2 in LPS-stimulated RAW 264.7 cells. EMM strongly suppressed nuclear translocation of NF-κB by preventing degradation of inhibitor of κB-α as well as by inhibiting phosphorylation of Akt and MAPKs. EMM reduced ear edema in PMA-induced mice. One of the anti-inflammatory compounds in EMM was identified as 6,6’-bieckol.ConclusionsThese results suggest that the anti-inflammatory properties of EMM are associated with the down-regulation of iNOS, COX-2, and pro-inflammatory cytokines through the inhibition of NF-κB pathway in LPS-stimulated macrophages.

Anti-inflammatory effects of phlorofucofuroeckol B-rich ethyl acetate fraction obtained from Myagropsis myagroides on lipopolysaccharide-stimulated RAW 264.7 cells and mouse edema.

Myagropsis myagroides has been used as a Chinese medicine and its extract has shown various biological activities, however, its anti-inflammatory mechanism remains unknown. In this study, we investigated the inhibitory effects of the ethyl acetate fraction of M. myagroides (EFM) on the production of inflammatory mediators and pro-inflammatory cytokines in lipopolysaccharides (LPS)-stimulated RAW 264.7 cells. EFM significantly inhibited LPS-induced production of nitric oxide (NO), prostaglandin E(2), and pro-inflammatory cytokines in a dose-dependent manner and suppressed the production of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 in RAW 264.7 cells. Inhibitory effect of EFM on iNOS expression and NO production was further confirmed using LPS-activated mouse peritoneal macrophages. EFM treatment strongly suppressed the activation of nuclear factor-kappa B (NF-κB) by suppressing phosphorylation of Akt and extracellular signal-regulated kinases (ERKs). EFM as well as phlorofucofuroeckol B (PFF-B), a major compound isolated from EFM, reduced ear edema induced by phorbol 12-myristate 13-acetate in mice. These results indicate that the anti-inflammatory effect of EFM, rich in PFF-B, on LPS-stimulated macrophages is regulated by the inhibition of NF-κB pathway through the inhibition of ERKs and Akt phosphorylation in LPS-stimulated macrophage cells.

Sargaquinoic acid attenuates inflammatory responses by regulating NF-κB and Nrf2 pathways in lipopolysaccharide-stimulated RAW 264.7 cells

Myagropsis myagroides, a brown alga, showed strong anti-inflammatory activities in the previous studies. In this study, we isolated a strong anti-inflammatory compound, sargaquinoic acid (SQA), from M. myagroides and investigated the anti-inflammatory action using lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. SQA suppressed the production of inducible nitric oxide synthase and cyclooxygenase-2 in LPS-stimulated cells as well as that of reactive oxygen species. As a result, SQA inhibited the production of NO, prostaglandin E2, and pro-inflammatory cytokines. LPS-induced transcriptional activation of nuclear factor-κB (NF-κB) was remarkably inhibited by SQA treatment through the prevention of inhibitor κB-α degradation. The regulation of NF-κB activation was also mediated by the phosphorylation of ERK and Akt in LPS-stimulated RAW 264.7 cells. Moreover, SQA induced the production of heme oxygenase 1 via activation of transcription factor Nrf2. These results indicate that SQA inhibits the LPS-induced expression of inflammatory mediators via suppression of ERK and Akt-mediated NF-κB pathway as well as up-regulation of Nrf2/HO-1 pathway, indicating that SQA has a potential therapeutic and preventive application in various inflammatory diseases.

Anti-inflammatory action of the ethanolic extract from Sargassum serratifolium on lipopolysaccharide-stimulated mouse peritoneal macrophages and identification of active components

Sargassum, a genus of brown algae (Phaeophyceae) in the Sargassaceae family, comprises approximately 400 species in the world. Among them, Sargassum serratifolium has been reported to have high level of meroterpenoids, which have antioxidant, anti-inflammatory, and neuroprotective activities. This study investigated the anti-inflammatory mechanism of ethanolic extract of S. serratifolium (ESS) in lipopolysaccharide (LPS)-stimulated peritoneal macrophages and identified anti-inflammatory compounds in ESS. ESS inhibited LPS-induced nitric oxide (NO) and prostaglandin E2 and the expression of inducible nitric oxide synthase and cyclooxygenase-2. ESS also reduced the release of pro-inflammatory cytokines in a dose-dependent manner. LPS-induced nuclear factor-κB transcriptional activity and translocation into the nucleus were significantly inhibited by ESS treatment through the prevention of the degradation of inhibitor κB-α. Furthermore, ESS inhibited the production of pro-inflammatory cytokines in mouse serum. The main anti-inflammatory components in ESS were identified as sargahydroquinoic acid, sargachromenol, and sargaquinoic acid based on the inhibition of NO production. Our results indicate that ESS can be used as a potential source of therapeutic agents for the treatment of inflammatory diseases.