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Hwang I.G.,Chungbuk National University | Kim H.Y.,Chungbuk National University | Woo K.S.,Functional Cereal Crop Research Division | Hong J.T.,Chungbuk National University | And 4 more authors.
Food Chemistry | Year: 2011

An α-glucosidase inhibitory substance was isolated and characterised from fructose-tyrosine Maillard reaction products (MRPs) and the inhibition mode of the active substance determined. The ethyl acetate fraction of fructose-tyrosine MRPs showed strong α-glucosidase inhibitory activity; this fraction was isolated and purified using silica gel column chromatography and semi-preparative RP-HPLC. The structure of the purified compound was determined using spectroscopic methods. The isolated compound was identified as 2,4-bis (p-hydroxyphenyl)-2-butenal (C16H14O3, HPB242). This is the first report of baker's yeast α-glucosidase inhibitory activity of HPB242 isolated from fructose-tyrosine MRPs. The IC 50 value of HPB242 on α-glucosidase inhibition was 4.00 ± 0.09 μg/ml. Kinetic data revealed that HPB242 inhibits the p-NPG hydrolysing activity of baker's yeast α-glucosidase noncompetitively with a Ki value of 0.870 mM. © 2011 Elsevier Ltd. All rights reserved.

Hwang I.G.,Chungbuk National University | Kim H.Y.,Chungbuk National University | Woo K.S.,Functional Cereal Crop Research Division | Lee J.,Chungbuk National University | Jeong H.S.,Chungbuk National University
Food Chemistry | Year: 2011

The various biological activities of Maillard reaction products (MRPs) from sugar (fructose and glucose) and 20 amino acid model systems were evaluated. Colour development, in vitro antioxidant, α-glucosidase inhibitory, antihypertensive, and antiproliferative activities of aqueous solutions of MRPs produced by heating at 130 °C for 2 h were measured. The fructose-amino acid mixture showed higher UV-absorbance and browning intensity than the glucose-amino acid mixture. The fructose-amino acid model MRPs showed higher DPPH and ABTS radical scavenging and ACE inhibitory activities than the glucose-amino acid model MRPs. The α-glucosidase inhibitory effect of MRPs derived from fructose- and glucose-tyrosine showed higher α-glucosidase inhibitory activity than that of other MRPs. Sugar-amino acid model MRPs inhibited the growth of HCT116 colon cancer cell in a dose-dependent manner (from 0.5 to 1.5 mg/ml). Glucose MRPs showed slightly higher antiproliferative activity than fructose MRPs. In particular, sugar-tryptophan and -tyrosine MRPs exerted higher biological activities than the other MRPs. © 2010 Elsevier Ltd. All rights reserved.

Nguyen D.H.,Catholic University of Daegu | Zhao B.T.,Catholic University of Daegu | Le D.D.,Catholic University of Daegu | Yoon Y.H.,Functional Cereal Crop Research Division | And 5 more authors.
Journal of Agricultural and Food Chemistry | Year: 2016

Two new fatty acid derivatives, echinochlorins A (8) and B (9) and a racemic lignan, (±)-anti-1-(4-hydroxy-3-methoxyphenyl)-2-{4-[(E)-3-acetoxypropen-1-yl]-2-methoxyphenoxy}propan-1,3-diol 3-acetate (1), were isolated from Echinochloa utilis grains, along with six known lignans (2-7) and two fatty acid derivatives (10, 11). Their structures were established by spectroscopic data analyses (IR, UV, HR-FABMS, GC-MS, and 1D and 2D NMR). The configuration of 1 was determined by Mosher's method. Compound 5 displayed potential inhibitory activity on lipopolysaccharide-induced NO production in macrophage RAW 264.7 cells with an IC50 value of 4.8 ± 0.5 μM. These isolated compounds in crude EtOH extract were also quantitated by HPLC. © 2016 American Chemical Society.

Woo H.J.,Kyungpook National University | Oh I.T.,Kyungpook National University | Lee J.Y.,Kyungpook National University | Jun D.Y.,Kyungpook National University | And 4 more authors.
Process Biochemistry | Year: 2012

Treatment of human promyelocytic leukemia HL-60 cells with apigeninidin could induce cytotoxicity (IC50 = ∼80 μM), along with apoptotic sub-G1 cells, TUNEL-positive apoptotic DNA fragmentation, activation of the multidomain pro-apoptotic Bcl-2 proteins (Bak and Bax), mitochondrial membrane potential (Δψm) loss, release of mitochondrial cytochrome c and AIF into the cytoplasm, activation of caspase-9, -3, -8, and -7, and cleavage of PARP and lamin B. These induced apoptotic events were accompanied by decrease of Bcl-2 level and increase of Bak and Bax levels. Apigeninidin-induced sub-G1 cells and activation of Bak and Bax were also detected in human acute leukemia Jurkat T cells, but not in Jurkat T cells overexpressing Bcl-2. Pretreatment of HL-60 cells with the pan-caspase inhibitor z-VAD-fmk reduced significantly apigeninidin-induced sub-G1 cells and caspase cascade activation, whereas it failed to suppress Bak and Bax activations, Δψm loss, and release of mitochondrial cytochrome c and AIF. None of FADD and caspase-8 deficiencies affected the sensitivity of Jurkat T cells to apigeninidin-induced cytotoxicity. These results demonstrated that apigeninidin-induced apoptosis was mediated by activation of Bak and Bax, mitochondrial damage and resultant release of not only cytochrome c, causing caspase cascade activation, but also caspase-independent death effector AIF in HL-60 cells. © 2012 Elsevier Ltd.

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