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Pleurotus florida has been widely used for nutritional and medicinal purposes. The present study was conducted to evaluate the antioxidant and anti-inflammatory effects of the fruiting bodies of P. florida extracted with acetone, methanol, and hot water. The antioxidant activities of the acetone and methanol extracts of P. florida showed stronger inhibition of ß-carotene-linoleic acid compared to that of the hot water extract. The acetone extract (8 mg/mL) showed a high reducing power of 1.86. The acetone and methanol extracts showed more effective DPPH radical scavenging activities than the hot water extract. The chelating effect of the extracts at lower concentrations was significantly effective compared to that of the positive control. Thirteen phenolic compounds were detected from acetonitrile and hydrochloric acid solvent extracts. Nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression in lipolysaccahride (LPS) stimulated RAW 264.7 cells, a murine macrophage cell line, were inhibited significantly by the mushroom extracts in a concentration dependent manner. The anti-inflammatory activity on carrageenan-induced edema in the rat hind-paw reduced significantly by the mushroom extracts. Therefore, we have demonstrated that P. florida fruiting bodies possess antioxidant and anti-inflammatory activites related to their inhibitory activities on NO production, iNOS protein expression, and carrageenan-induced paw edema in rats. The results suggest that the fruiting bodies of P. florida are a good source of natural antioxidant and anti-inflammatory agents.

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Coumarins comprise a group of natural phenolic compounds found in a variety of plant sources. Protective effects of coumarins against cytotoxicity induced by linoleic acid hydroperoxide were examined in cultured human umbilical vein endothelial cells. When the cells were incubated in medium supplemented with linoleic acid hydroperoxide and coumarins, esculetin (6,7-dihydroxycoumarin) and 4-methylesculetin protected cells from injury by linoleic acid hydroperoxide. Fraxetin and caffeic acid showed weak, but significant, protection. Esculin as well as esculetin and 4-methylesculetin were effective for protecting cells against linoleic acid hydroperoxide-induced cytotoxicity in the case of pretreatment for 24 h, however fraxetin and caffeic acid showed no protection. Since esculetin was detected after 24 h treatment with esculin, a sugar moiety in the esculin molecule appears to be hydrolyzed during pretreatment. Coumarins such as umbelliferone containing only one hydroxyl group showed no protective effect in pretreatment or concurrent treatment. Esculetin and 4-methylesculetin provided synergistic protection against cytotoxicity induced by linoleic acid hydroperoxide with alpha-tocopherol. Furthermore, the radical-scavenging ability of coumarins was examined in electron spin resonance spectrometry. Esucletin, 4-methylesculetin, fraxetin, and caffeic acid showed the quenching effect on the 1,1-diphenyl-2-picrylhydrazyl radical. These results indicate that the presence of an ortho catechol moiety in the coumarin molecules plays an important role in the protective activities against linoleic acid hydroperoixde-induced cytotoxicity.

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The intestinal uptake of [1-14C]linolenic acid [18:3(n-3)], an essential fatty acid, was investigated in isolated hamster intestinal cells using a rapid filtration method and 20 mmol/L taurocholate as solubilizing agent. Under these conditions, the initial rate of alpha-linolenic acid uptake was not a linear function of external monomer concentrations in the range of 2 to 2250 nmol/L, but rather the transport system was characterized by saturation kinetics with Vmax = 11.37 nmol.mg protein-1.min-1 and Km = 382 nmol/L. Temperature and metabolic poisons (2,4-dinitrophenol, antimycin A) drastically decreased the initial rate of uptake, as did replacement of Na+. The presence of excess unlabeled alpha-linolenic acid in the incubation medium significantly inhibited the uptake of [1-14C]linolenic acid, whereas L-alanine and D-glucose had no effect. Other long-chain fatty acids (saturated or unsaturated), as well as cholesterol, inhibited the uptake of [1-14C]linolenic acid. We concluded that an active, carrier-mediated mechanism was involved in the intestinal transport of alpha-linolenic acid. Inhibition data are compatible with the hypothesis that intestinal uptake of alpha-linolenic acid is mediated by a carrier common to long-chain fatty acids.

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The inhibition of coagulase-negative staphylococci and Staphylococcus aureus of human or animal origin by most free fatty acids was similar, but coagulase-positive staphylococci were sensitive and coagulase-negative cultures were resistant to linolenic acid. Animal strains of S. aureus were more sensitive to linolenic acid than were human strains. These differences were reflected in the relative abilities of the three categories of strains to survive on human skin. The antibacterial effects of 20 mg of linolenic acid were inactivated by 1 ml of serum in vitro. A test organism seeded on to skin also survived better if first suspended in serum. The mechanism of the interaction between serum and linolenic acid may be due to a detergent effect of the serum and could account for colonisation of diseased skin with S. aureus. Cultures of S. aureus seeded on to human skin were rapidly killed after the skin has been covered with linolenic acid. The possibility of therapeutic use of linolenic acid as an antibacterial agent should be explored.

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