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        Hyperglycemia and Anthocyanin Inhibit Quercetin Metabolism in HepG2 Cells

        Naoto Hashimoto,Jeffrey B. Blumberg,C-Y. Oliver Chen 한국식품영양과학회 2016 Journal of medicinal food Vol.19 No.2

        A high glucose (Glu) milieu promotes generation of reactive oxygen species, which may not only cause cellular damage, but also modulate phase II enzymes that are responsible for the metabolism of flavonoids. Thus, we examined the effect of a high Glu milieu on quercetin (Q) metabolism in HepG2 cells. HepG2 cells were grown for 3 days in Glu ranging from 5.5 to 50 mmol/L and/or cyanidin-3-glucoside (C3G) ranging from 0 to 25 μmol/L. Subsequently, the capacity of HepG2 cells to metabolize Q was assessed for up to 16 h. Q metabolites were analyzed by high-performance liquid chromatography. Four major Q metabolites were observed in the culture medium and inside the HepG2 cells. Three of these metabolites appear to be sulfated forms of Q or methylated Q, and one was a methylated Q. These metabolites and Q itself were reduced or tended to be reduced in cells grown in a high Glu compared to a normal Glu medium. Addition of C3G or superoxide dismutase plus catalase did not prevent or enhance reduction of Q metabolites. In vitro, a hyperglycemic milieu decreases the production of the principal Q metabolites in HepG2 cells, mediated through mechanisms independent of oxidative stress.

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        Effect of Colored Potato Flakes Against Acetaminophen-induced Liver Damage in Rats

        Kiyoshi Ohba,Shoko Watanabe,Kyu-Ho Han,Naoto Hashimoto,Takahiro Noda,Ken-ichiro Shimada,Hisashi Tanaka,Mitsuo Sekikawa,Michihiro Fukushima 한국식품과학회 2007 Food Science and Biotechnology Vol.16 No.3

        We examined the hepatoprotective effects of colored potato flakes on acetaminophen(AAP)-induced liver damage in rats. F344/DuCrj (8 week-old) rats were fed a cholesterol-free diet with 54,9486 g of α-corn starch/100 g diet and were orally treated with 25% colored flakes of Kitamurasaki (KM: light purple), Northern Ruby (NR: red), and Queen (SQ: medium purple) potatoes co-administered with AAP (0.5 g/100 g diet)for 4 weeks. The hepatic thiobarbituric acid-reactive substances (TBARS) values in the KM, NR, and SQ group were significantly lower (p<0.05) than those in the control groups with and wothout AAP. Furthermore, the hepatic catalase, Mn-superoxide dismutase (SOD), and Cu/Zn-SOD mRNA levels in the KM, NR, and SQ groups were higher than those in the control groups with and without AAP. The present findings suggest that colored potato flakes are useful as a prophylactic agent against oxidative liver damage.

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        Hepatoprotective Effects of Potato Peptide against D-Galactosamineinduced Liver Injury in Rats

        Kiyoshi Ohba,Kyu-Ho Han,Ruvini Liyanage,Megumi Nirei,Naoto Hashimoto,Ken-ichiro Shimada,Mitsuo Sekikawa,Keiko Sasaki,Chi-Ho Lee,Michihiro Fukushima 한국식품과학회 2008 Food Science and Biotechnology Vol.17 No.6

        The effect of some peptides on hepatoprotection and cecal fermentation against D-galactosamine (GalN)-treated rats was studied. In acute hepatic injury tests, serum alanine aminotransferase (ALT), aspartate aminotranferase (AST), and lactic dehydrogenase (LDH) activities were remarkably increased after injection of GalN. However, potato and soybean peptides significantly decreased GalN-induced alterations of serum ALT and AST activities. Hepatic thiobarbituric acidreactive substance (TBARS) concentration in GalN-treated groups fed potato and soybean peptides was significantly lower than that in GalN-treated control group. Hepatic glutathione level in the GalN-treated group fed potato peptide was significantly higher than that in GalN-treated control group. Furthermore, cecal Lactobacillus level in GalN-treated groups fed potato and soybean peptides was significantly higher than that in GalN-treated control group, and cecal short-chain fatty acid concentrations in GalN-treated group fed potato peptide were significantly higher than in GalN-treated control group. These results indicate that potato peptide may improve the cecal fermentation and prevent the GalN-induced liver damage in rats.

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