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BackgroundThe high morbidity of metabolic dysfunction diseases has heightened interest in seeking natural and safe compounds to maintain optimal health. γ-Oryzanol (OZ), the ferulic acid (FA) ester with phytosterols, mainly present in rice bran has been shown to improve markers of metabolic syndrome. This study investigates the effects of FA and OZ on alleviating high-fat and high-fructose diet (HFFD)-induced metabolic syndrome parameters.MethodsMale SD rats were fed with a regular rodent diet, HFFD, or HFFD supplemented with 0.05% FA or 0.16% OZ (equimolar concentrations) for 13 weeks. Food intake, organ indices, serum lipid profiles, glucose metabolism, insulin resistance (IR) index and cytokine levels were analyzed. The mechanisms were further investigated in oleic acid-stimulated HepG2 cells by analyzing triglyceride (TG) content and lipogenesis-related gene expressions.ResultsIn the in vivo study, FA and OZ exhibited similar effects in alleviating HFFD-induced obesity, hyperlipidemia, hyperglycemia, and IR. However, only OZ treatment significantly decreased liver index and hepatic TG content, lowered serum levels of C-reactive protein and IL-6, and increased serum concentration of adiponectin. In the in vitro assay, only OZ administration significantly inhibited intracellular TG accumulation and down-regulated expression of stearoyl coenzyme-A desaturase-1, which might facilitate OZ to enhance its hepatoprotective effect.ConclusionOZ is more effective than FA in inhibiting hepatic fat accumulation and inflammation. Thus, FA and OZ could be used as dietary supplements to alleviate the deleterious effects of HFFD.

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The aim of present work was to investigate the effect of solid-state fermentation with filamentous fungi (Aspergillus oryzae var. effuses, Aspergillus oryzae, and Aspergillus niger) on total phenolics content (TPC), flavonoids, and antioxidant activities of four subfractions of oat, namely, n-hexane, ethyl acetate (EA), n-butanol, and water, and compare them to their corresponding subfractions of unfermented oat. The TPC and total flavonoids increased dramatically, especially in EA subfractions (p < 0.05). The levels of antioxidant activity of subfractions were also significantly enhanced (p < 0.05). The highest antioxidant activities were also found in the EA subfractions. The polyphenols in EA were analyzed by high-performance liquid chromatography at 280 nm. Most polyphenols were increased remarkably, especially ferulic and caffeic acids. There was a clear correlation between the TPC and antioxidant activity. In conclusion, fungi fermentation is a potential bioprocess for increasing the TPC, flavonoids, and antioxidant activities of oat-based food.

This model easily recovers with normal diet feeding. A high-fat diet is suggested as the background diet in future pharmacological studies using this model.

Retinal pigment epithelium (RPE) cells are vital for retinal health. However, they are susceptible to injury with ageing and exposure to excessive light, including UV (100-380 nm) and visible (380-760 nm) radiation. To evaluate the protective effect of blueberry anthocyanins on RPE cells, in vitro cell models of replicative senescent and light-induced damage were established in the present study. After purification and fractionation, blueberry anthocyanin extracts (BAE) were yielded with total anthocyanin contents of 31·0 (SD 0·5) % and were used in this study. Replicative senescence of RPE cells was induced by repeatedly passaging cells from the fourth passage to the tenth. From the fifth passage, cultured RPE cells began to enter a replicative senescence, exhibiting reduced cell proliferation along with an increase in the number of β-galactosidase-positive cells. RPE cells maintained high cell viability (P < 0·01) and a low (P < 0·01) percentage of β-galactosidase-positive cells when treated with 0·1 μg/ml BAE. In contrast, after exposure to 2500 (SD 500) lx light (420-800 nm) for 12 h, RPE cells in the positive control (light exposure, no BAE treatment) exhibited premature senescence, low (P < 0·01) cell viability and increased (P < 0·01) vascular endothelial growth factor (VEGF) release compared with negative control cells, which were not subjected to light irradiation and BAE exposure. Correspondingly, BAE is beneficial to RPE cells by protecting these cells against light-induced damage through the suppression of ageing and apoptosis as well as the down-regulation of the over-expressed VEGF to normal level. These results demonstrate that BAE is efficacious against senescence and light-induced damage of RPE cells.

This study aimed to investigate the protective effect of genistein or puerarin on chronic alcohol-induced liver injury in vivo and to explore the underlying mechanisms of hepatoprotective effects. Mice were administered genistein or puerarin (0.3 mmol kg(-1) body weight) and gastrically infused with 50% alcohol once per day for 5 weeks. Levels of serum transaminases, serum and hepatic lipids, hepatic antioxidant capacities, inflammation, apoptosis, and histopathological sections were analyzed. Results showed that genistein and puerarin exhibited similar effects in ameliorating alcohol-induced liver injury. However, genistein is more effective than puerarin in decreasing levels of malondialdehyde (1.05 ± 0.0947 vs 1.28 ± 0.213 nmol/mg pro, p < 0.05), tumor necrosis factor α (3.12 ± 0.498 vs 3.82 ± 0.277 pg/mg pro, p < 0.05), interleukin-6 (1.46 ± 0.223 vs 1.88 ± 0.309 pg/mg pro, p < 0.05), whereas puerarin is more effective than genistein in ameliorating serum activities or levels of alanine transaminase (35.8 ± 3.95 vs 42.6 ± 6.56 U/L, p < 0.05) and low-density lipoprotein cholesterol (1.12 ± 0.160 vs 1.55 ± 0.150 mmol/L, p < 0.05). In conclusion, both genistein and puerarin effectively alleviate hepatic damage induced by chronic alcohol administration through potential antioxidant, anti-inflammatory, or anti-apoptotic mechanisms.