Fucoidan is an l-fucose-enriched sulfated polysaccharide isolated from brown algae and marine invertebrates. In this study, we investigated the protective effect of fucoidan from Fucus vesiculosus on alcohol-induced murine liver damage. Liver injury was induced by oral administration of 25% alcohol with or without fucoidan (30 mg/kg or 60 mg/kg) for seven days. Alcohol administration increased serum aspartate aminotransferase and alanine aminotransferase levels, but these increases were suppressed by the treatment of fucoidan. Transforming growth factor beta 1 (TGF-β1), a liver fibrosis-inducing factor, was highly expressed in the alcohol-fed group and human hepatoma HepG2 cell; however, the increase in TGF-β1 expression was reduced following fucoidan administration. Treatment with fucoidan was also found to significantly reduce the production of inflammation-promoting cyclooygenase-2 and nitric oxide, while markedly increasing the expression of the hepatoprotective enzyme, hemeoxygenase-1, on murine liver and HepG2 cells. Taken together, the antifibrotic and anti-inflammatory effects of fucoidan on alcohol-induced liver damage may provide valuable insights into developing new therapeutics or interventions.

Obesity is a metabolic disorder developed by overnutrition and a major cause for insulin resistance and cardiovascular events. Since adipose tissue is one of the major sites for the synthesis and secretion of cytokines, enlarged adipose tissue in obese condition alters inflammatory state leading to pathophysiological conditions such as type 2 diabetes and increased cardiovascular risk. A plausible theory for development of metabolic dysregulation is that obesity increases secretion of inflammatory cytokines from adipose tissue and causes a chronic inflammation in the whole body. Additionally accumulation of lipids in non-adipose tissues elevates the cellular levels of bioactive lipids that inhibit the signaling pathways implicated in metabolic regulation together with activated inflammatory response. Recent findings suggest that obesity-induced inflammatory response leads to modulation of sphingolipid metabolism and these bioactive lipids may function as mediators for increased risk of metabolic dysfunction. Importantly, elucidation of mechanism regarding sphingolipid metabolism and inflammatory disease will provide crucial information to development of new therapeutic strategies for the treatment of obesity-induced pathological inflammation.

Angelica gigas (AG) is effective against various medical conditions such as bacterial infection, inflammation, and cancer. It contains a number of coumarin compounds and the group of interest is the pyranocoumarin, which comprises decursin and decursinol angelate. This group has an effect on controlling inflammation, which is caused by excessive nitric oxide (NO) production. Heme oxygenases (HOs), particularly HO-1, play a role in regulating the production of NO. Thus, this study aimed to investigate the anti-inflammatory effects of AG by measuring HO-1 expression. Treatments with CH₂Cl₂ layer and Angelica gigas extract (AGE) showed the highest NO inhibition effects. Decursin, decursinol angelate, and nodakenin were isolated from the CH₂Cl₂ layer of AGE. Decursin also demonstrated the highest anti-oxidative effect among the coumarins. Although decursin had the best NO inhibition and anti-oxidative effects, the effects of AGE treatment far surpassed that of decursin. This is owing to the combination effect of the coumarins present within AGE, which is a solvent extract of AG. The expression of HO-1 is an effective indicator of the anti-inflammatory effects of AG. Based on the results of the coumarin compounds, HO-1 expression was found to be dose dependent and specific to decursin.

Sixteen arene–Ru based molecular-rectangles were self-assembled in high yields by the equimolar mixing of arene–Ru acceptors (Aa–Ad) with various azopyridyl ligands (1,2-di(pyridyl-4yl)diazene (L1), 1,2-bis(pyridin-4-ylmethylene)hydrazine (L2), 1,2-bis(1-(pyridin-4-yl)ethylidene)hydrazine (L3), 1,2-bis(pyridin-4-ylmethylene)hydrazine (L4)) in nitromethane–methanol solutions. These new molecular-rectangles were fully characterized by a host of analytical techniques including elemental analysis, ¹H and ¹³C NMR and HR-ESI-MS. The solid-state structures of two molecular-rectangles (1b and 4d) were determined by single crystal X-ray diffraction data. UV-visible and fluorescence studies were also carried out for the entire suite of rectangles. As with recent studies of similar arene–Ru complexes, the anti-proliferative activities of these complexes were evaluated against SK-hep-1 (liver cancer) and A-549 (lung cancer) human cancer lines. Additionally, the cellular pharmacology and intracellular localizations in AGS (gastric cancer) human cancer cells were determined for selected complexes (1c, 1d and 4c) by apoptosis and fluorescence microscopy studies. These studies confirm that arene–Ru molecular-rectangles inhibit cell cycle progression to the G0 phase, in contrast to that of cisplatin which arrests cell growth in the G2 phase.