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Lee C.-L.,National Taitung University | Hung Y.-P.,National Taitung University | Hsu Y.-W.,Sunway Biotechnology Company Ltd | Pan T.-M.,National Taiwan University of Science and Technology
Journal of Agricultural and Food Chemistry | Year: 2013

Monacolin K has long been considered a major effective component in the hypolipidemic functions of Monascus. Monacolin K also serves as a well-known hypolipidemic medication, but its side effect myopathy is a concern. Monascin and ankaflavin, the yellow pigments produced by Monascus species, have been proven to possess hypolipidemic functions; however, no studies have compared the hypolipidemic effects of monascin, ankaflavin, and monacolin K under the same dosages. In this study, the equal dosages of monascin, ankaflavin, and monacolin K were oral administrated to hamsters fed a high cholesterol diet for 6 weeks. Comparison of the displayed hypolipidemic and anti-atherosclerosis effects was performed, in addition to an investigation into the inducement of side effect. The results indicated that monascin and ankaflavin were similar to monacolin K in significantly reducing total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) levels in serum and lipid plaque (p < 0.05) in the heart aorta. In addition, ankaflavin achieved the effects of serum TC and TG reduction, with no significant difference as compared to those effects of monacolin K (p > 0.05). However, as compared to monacolin K, ankaflavin possessed more significant effects on the prevention of fatty liver and lipid plaque accumulation in heart aorta. More importantly, monascin significantly enhanced high-density lipoprotein cholesterol (HDL-C) concentrations, while monacolin K displayed the opposite effect. Regarding the side effect, monacolin K also raised elevated creatinine phosphokinase (CPK) activity, which was highly correlated with rhabdomyolysis development, while monascin and ankaflavin did not induce such a side effect. In conclusion, MS and AK had the potential to be developed as hypolipidemic agents without rhabdomyolysis development. © 2012 American Chemical Society. Source


Lee B.-H.,National Taiwan University of Science and Technology | Hsu W.-H.,National Taiwan University of Science and Technology | Hsu Y.-W.,Sunway Biotechnology Company Ltd | Pan T.-M.,National Taiwan University of Science and Technology
Journal of Functional Foods | Year: 2013

The effects of dimerumic acid (DMA) on apoptosis prevention and insulin production in the glucose metabolite methylglyoxal (MG)-treated pancreatic RINm5F cells were evaluated. MG was found to induce apoptotic signal molecules mediated by oxidative stress in RINm5F cells, including caspase-3 and caspas-9, resulting in cell death and decreasing insulin production. In addition, DMA elevated insulin synthesis via up-regulating mammalian homologue of avian MafA/L-Maf (Maf-A) and pancreatic-duodenal homeobox-1 (PDX-1) and inhibited MG-mediated CCAAT/enhancer binding proteins-β (C/EBPβ) expression, which is a negative regulator for insulin production. Nuclear factor-erythroid2-related factor 2 (Nrf2) is essential for antioxidant responsive element (ARE)-mediated induction. Results indicated that nuclear translocation of Nrf2 was promoted by DMA in MG-treated RINm5F cells to increase heme oxygenase-1 (HO-1) and glutamate-cysteine ligase (GCL) expressions. We confirmed that DMA protected PDX-1, Maf-A, and insulin production against MG-induced oxidative stress mediating by Nrf2 in Nrf2-knockdown RINm5F cells. These results suggest that DMA exerts antioxidative ability to attenuate MG-induced pancreatic cell damage and elevates insulin level to improve diabetes. © 2013 Elsevier Ltd. Source


Lee B.-H.,National Taiwan University of Science and Technology | Hsu W.-H.,National Taiwan University of Science and Technology | Huang T.,National Taiwan University of Science and Technology | Chang Y.-Y.,National Taiwan University of Science and Technology | And 2 more authors.
Journal of Agricultural and Food Chemistry | Year: 2013

Hyperglycemia is associated with advanced glycation end products (AGEs). This study was designed to evaluate the inhibitory effects of monascin on receptor for advanced glycation end product (RAGE) signal and THP-1 monocyte inflammation after treatment with S100b, a specific ligand of RAGE. Monascin inhibited cytokine production by S100b-treated THP-1 monocytes via up-regulation of nuclear factor-erythroid 2-related factor-2 (Nrf2) and alleviated p47phox translocation to the membrane. Methylglyoxal (MG, 600 mg/kg bw) was used to induce diabetes in Wistar rats. Inhibitions of RAGE and p47phox by monascin were confirmed by peripheral blood mononuclear cells (PBMCs) of MG-induced rats. Silymarin (SM) was used as a positive control group. It was found that monascin promoted heme oxygenase-1 (HO-1) expression mediated by Nrf2. Suppressions of AGEs, tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-β) in serum of MG-induced rats were attenuated in the monascin administration group treated with retinoic acid (RA). RA treatment resulted in Nrf2 inactivation by increasing RA receptor-α (RARα) activity, suggesting that RA acts as an inhibitor of Nrf2. The results showed that monascin exerted anti-inflammatory and antioxidative effects mediated by Nrf2 to prevent the development of diseases such as type 2 diabetes caused by inflammation. © 2013 American Chemical Society. Source


Hsu W.-H.,National Taiwan University of Science and Technology | Chen T.-H.,National Taiwan University of Science and Technology | Lee B.-H.,National Taiwan University of Science and Technology | Hsu Y.-W.,Sunway Biotechnology Company Ltd | Pan T.-M.,National Taiwan University of Science and Technology
Food and Chemical Toxicology | Year: 2014

Yellow pigments monascin (MS) and ankaflavin (AK) are secondary metabolites derived from Monascus-fermented products. The hypolipidemic and anti-inflammatory effects of MS and AK indicate that they have potential on preventing or curing nonalcoholic fatty liver disease (NAFLD). Oleic acid (OA) and high-fat diet were used to induce steatosis in FL83B hepatocytes and NAFLD in mice, respectively. We found that both MS and AK prevented fatty acid accumulation in hepatocytes by inhibiting fatty acid uptake, lipogenesis, and promoting fatty acid beta-oxidation mediated by activating peroxisome proliferator-activated receptor (PPAR)-α and AMP-activated kinase (AMPK). Furthermore, MS and AK significantly attenuated high-fat diet-induced elevation of total cholesterol (TC), triaceylglycerol (TG), free fatty acid (FFA), and low density lipoprotein-cholesterol (LDL-C) in plasma. MS and AK promoted AMPK phosphorylation, suppressed the steatosis-related mRNA expression and inflammatory cytokines secretion, as well as upregulated farnesoid X receptor (FXR), peroxisome proliferator-activated receptor gamma co-activator (PGC)-1α, and PPARα expression to induce fatty acid oxidation in the liver of mice. We provided evidence that MS and AK act as PPARα agonists to upregulate AMPK activity and attenuate NAFLD. MS and AK may be supplied in food supplements or developed as functional foods to reduce the risk of diabetes and obesity. © 2013 Elsevier Ltd. Source


Lee C.-L.,National Taitung University | Kuo T.-F.U.,National Taiwan University | Wu C.-L.,Sunway Biotechnology Company Ltd | Wang J.-J.,Fooyin University | Pan T.-M.,National Taiwan University
Journal of Agricultural and Food Chemistry | Year: 2010

Amyloid beta (Aβ) peptide is closely related to the onset of Alzheimer's disease (AD). A high-cholesterol or high-energy diet was demonstrated to stimulate Aβ formation and deposition in the amyloid precursor protein (APP) pathway and, oppositely, downregulate the secretion of the neuroprotective soluble APP α-fragment (sAPPα). Wonascus-fermented red mold rice (RMR) Including multiple cholesterol-lowering agents, antioxidants, and anti-inflammatory agents has been proven to ameliorate Aβ40 infusion-Induced memory deficit in our previous study. In this study, the ethanol extract of RMR (RE) and natural RMR were respectively tested for their effect on the mediation of the proteolytic process of APP in cholesterol-treated human neuroblastoma IMR32 cell, as well as their effect on memory and learning ability and the expression of AD risk factors in intracerebroventricular Aβ40-infused hyperlipidemic rats. In the results, RE suppressed cholesterolraised -secretase activity and further resulted in the increase of sAPPα secretion in the IMR32 cell. In the animal test, RMR potently reversed the memory deficit in the water maze and passive avoidance tasks. RMR administration could prevent against Aβ40 infusion plus the great damage caused by a high energy diet in hippocampus and cortex involved in the raise of thiobarbituric acid reactive substances and reactive oxygen species. The neuroprotection provided by RMR downregulates Aβ40 formation and deposition by suppressing the cholesterol-raised β-secretase activity and apollpoprotein E expression, as well as mediates the proteolytic process of APP toward neuroprotective sAPPα secretion in hippocampus. ©2010 American Chemical Society. Source

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