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Objective: The aim of this study was to characterize the exopolysaccharides (EPS)-producing lactic acid bacteria from Taiwanese ropy fermented milk (TRFM) for developing a clean label low-fat fermented milk.Methods: Potential isolates from TRFM were selected based on the Gram staining test and observation of turbid suspension in the culture broth. Random amplified polymorphic DNA-polymerase chain reaction, 16S rRNA gene sequencing, and API CHL 50 test were used for strain identification. After evaluation of EPS concentration, target strains were introduced to low-fat milk fermentation for 24 h. Fermentation characters were checked: pH value, acidity, viable count, syneresis, and viscosity. Sensory evaluation of fermented products was carried out by 30 volunteers, while the storage test was performed for 21 days at 4°C.Results: Two EPS-producing strains (APL15 and APL16) were isolated from TRFM and identified as Lactococcus (Lc.) lactis subsp. cremoris. Their EPS concentrations in glucose and lactose media were higher than other published strains of Lc. lactis subsp. cremoris. Low-fat fermented milk separately prepared with APL15 and APL16 reached pH 4.3 and acidity 0.8% with a viable count of 9 log colony-forming units/mL. The physical properties of both products were superior to the control yogurt, showing significant improvements in syneresis and viscosity (p

There is accumulating evidence that LDL oxidation is essential for atherogenesis and antioxidants that prevent oxidation may either decelerate or reduce atherogenesis. Current study focused on the effect and mechanism of 3',4'-dihydroxy-5,6,7,8-tetramethoxyflavone (DTF), a major metabolite of nobiletin (NOB, a citrus polymethoxylated flavone) on atherogenesis. We found DTF had stronger inhibitory activity than alpha-tocopherol on inhibiting Cu2+-mediated LDL oxidation measured by thiobarbituric acid-reactive substances assay (TBARS), conjugated diene formation and electrophoretic mobility. Monocyte-to-macrophage differentiation plays a vital role in early atherogenesis. DTF (10-20 microM) dose-dependently attenuated differentiation along with the reduced gene expression of scavenger receptors, CD36 and SR-A, in both PMA- and oxidized low-density lipoprotein (oxLDL)-stimulated THP-1 monocytes. Furthermore, DTF treatment of monocytes and macrophages led to reduction of fluorescent DiI-acLDL and DiI-oxLDL uptake. In conclusion, at least three mechanisms are at work in parallel: DTF reduces LDL oxidation, attenuates monocyte differentiation into macrophage and blunts uptake of modified LDL by macrophage. The effect is different from that of NOB, from which DTF is derived. This study thus significantly enhanced our understanding on how DTF may be beneficial against atherogenesis.

Dietary flavonoid intake has been reported to be inversely associated with the incidence of coronary artery disease. To clarify the possible role of flavonoids in the prevention of atherosclerosis, we investigated the effects of some of these compounds, including fisetin, morin and myricetin, on the susceptibility of low-density lipoprotein (LDL) to oxidative modification and on oxLDL uptake in macrophages. The results demonstrated that fisetin had stronger inhibitory activity than the other two on inhibiting Cu(2+)-mediated LDL oxidation measured by thiobarbituric acid-reactive substances assay (TBARS), conjugated diene formation and electrophoretic mobility. The class B scavenger receptor, CD36, to which oxLDL binds, is present in atherosclerotic lesions. Treatment of U937-derived macrophages with myricetin (20 microM) significantly inhibited CD36 cell surface protein and mRNA expression (p0.01). Fisetin, morin and myricetin (20 microM) also reduced the feed-forward induction of CD36 mRNA and surface protein expression by PPARgamma. The inhibition of CD36 by flavonols was mediated by interference with PPARgamma activation thus counteracting the deleterious autoamplification loop of CD36 expression stimulated by PPARgamma ligand. All three flavonols (10 and 20 microM) markedly decreased the uptake of 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanide perchlorate (DiI)-labeled oxLDL uptake in U937-derived macrophages dose-dependently. Current evidences indicate that fisetin, morin and myricetin not only prevent LDL from oxidation but also block oxLDL uptake by macrophages at least in part through reducing CD36 gene expression on macrophages. In conclusion, flavonols may play a role in ameliorating atherosclerosis.

Scope: Nobiletin, a polymethoxyflavone from the peel of citrus fruits, has been reported to inhibit modified LDL uptake in macrophages and enhance hepatic LDL receptor expression and activity. We report the anti-atherogenic effect and mechanism of 5-demethylnobiletin, an auto-hydrolysis product of nobiletin. Methods and results: 5-Demethylnobiletin significantly attenuated phorbol 12-myristate 13-acetate-induced gene expression and activity of scavenger receptors, CD36, scavenger receptor-A and lectin-like oxidized LDL receptor-1. The inhibitory effect is partly associated with the inhibition of protein-kinase C activity and c-Jun NH2-terminal kinase 1/2 phosphorylation, thereby inhibiting the activation of activator protein-1 and nuclear factor-κB. 5-Demethylnobiletin treatment also led to reduction of oxidized LDL-induced CD36 mRNA expression and blockade of 1,1′-dioctadecyl-3,3,3′,3′-tetramethylindocarbocyanide perchlorate-modified LDL uptake in THP-1-derived macrophages. In the human hepatoma cell line HepG2, 5-demethylnobiletin significantly induced LDL receptor activity and transcription, at least in part, through steroid-response element-binding protein-2 activation. 5-Demethylnobiletin also decreased the mRNA expression of acyl CoA:diacylglycerol acyltransferase 2, the key enzyme involved in the hepatic triacylglycerol biosyntheses. Conclusion: Current results suggest that 5-demethylnobiletin has diverse anti-atherogenic bioactivities. It is more potent in inhibiting monocyte-to-macrophage differentiation and foam cell formation than its permethoxylated counterpart, nobiletin. It exhibits similar hypolipidemic activity as nobiletin and both can enhance LDL receptor gene expression and activity and decreased acyl CoA:diacylglycerol acyltransferase 2 expression.