• Biomolecules & Therapeutics
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• 제24권1호
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• pp.49-56
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• 2016

To determine the protective effect of aloe-emodin (AE) from high glucose induced toxicity in RIN-5F (pancreatic ${\beta}$-cell) cell and restoration of its function was analyzed. RIN-5F cells have been cultured in high glucose (25 mM glucose) condition, with and without AE treatment. RIN-5F cells cultured in high glucose decreased cell viability and increased ROS levels after 48 hr compared with standard medium (5.5 mM glucose). Glucotoxicity was confirmed by significantly increased ROS production, increased pro-inflammatory (IFN-${\gamma}$, IL-$1{\beta}$,) & decreased anti-inflammatory (IL-6&IL-10) cytokine levels, increased DNA fragmentation. In addition, we found increased Bax, caspase 3, Fadd, and Fas and significantly reduced Bcl-2 expression after 48 hr. RIN-5F treated with both high glucose and AE ($20{\mu}M$) decreased ROS generation and prevent RIN-5F cell from glucotoxicity. In addition, AE treated cells cultured in high glucose were transferred to standard medium, normal responsiveness to glucose was restored within 8hr and normal basal insulin release within 24 hr was achieved when compared to high glucose.

• Nutrition Research and Practice
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• 제9권6호
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• pp.586-591
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• 2015

BACKGROUND/OBJECTIVES: Reactive oxygen species (ROS) formation is closely related to miconazole-induced heart dysfunction. Although rhamnetin has antioxidant effects, it remained unknown whether it can protect against miconazole-induced cardiomyocyte apoptosis. Thus, we investigated the effects of rhamnetin on miconazole-stimulated H9c2 cell apoptosis. MATERIALS/METHODS: Cell morphology was observed by inverted microscope and cell viability was determined using a WelCount$^{TM}$ cell proliferation assay kit. Miconazole-induced ROS production was evaluated by fluorescence-activated cell sorting with 6-carboxy-2',7'-dichlorofluoroscein diacetate ($H_2DCF$-DA) stain. Immunoblot analysis was used to determine apurinic/apyrimidinic endonuclease 1 (APE/Ref-1) and cleaved cysteine-aspartic protease (caspase) 3 expression. NADPH oxidase levels were measured using real-time polymerase chain reaction. RESULTS: Miconazole (3 and $10{\mu}M$) induced abnormal morphological changes and cell death in H9c2 cells. Rhamnetin enhanced the viability of miconazole ($3{\mu}M$)-treated cells in a dose-dependent manner. Rhamnetin (1 and $3{\mu}M$) treatment downregulated cleaved caspase 3 and upregulated APE/Ref-1 expression in miconazole-stimulated cells. Additionally, rhamnetin significantly reduced ROS generation. CONCLUSIONS: Our data suggest that rhamnetin may have cytoprotective effects in miconazole-stimulated H9c2 cardiomyocytes via ROS inhibition. This effect most likely occurs through the upregulation of APE/Ref-1 and attenuation of hydrogen peroxide levels.

• Preventive Nutrition and Food Science
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• 제16권4호
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• pp.299-306
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• 2011

The present study was designed to evaluate the inhibitory effects of fermented Liriope platyphylla extract on the production of inflammation-related mediators (NO, ROS, NF-${\kappa}B$, iNOS and COX-2) and pro-inflammatory cytokines (TNF-${\alpha}$, IL-$1{\beta}$, IL-6) in lipopolysaccharide-stimulated RAW 264.7 macrophages. Freeze-dried Liriope platyphylla was fermented by Saccharomyces cerevisiae and extracted with 70% ethanol. In lipopolysaccharide-stimulated macrophage cells, the treatment with fermented Liriope platyphylla extract decreased the generation of intracellular reactive oxygen species dose-dependently and increased antioxidant enzyme activities, including superoxide dismutase, catalase and glutathione peroxidase. Fermented Liriope platyphylla extract also inhibited NO production in lipopolysaccharide-stimulated RAW 264.7 cell. The expressions of NF-${\kappa}B$, iNOS, COX-2 and pro-inflammatory cytokines were inhibited by the treatment with fermented Liriope platyphylla extract. Thus, this study shows the fermented Liriope platyphylla extract could be effective at inhibiting the inflammation process.

• Preventive Nutrition and Food Science
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• 제21권1호
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• pp.31-37
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• 2016

Opuntia humifusa (OHF) has been used as a nutraceutical source for the prevention of chronic diseases. In the present study, the inhibitory effects of ethyl acetate extracts of OHF on the proliferation of AGS human gastric cancer cells and the mode of action were investigated. To elucidate the antiproliferative mechanisms of OHF in cancer cells, the expression of genes related to apoptosis and cell cycle arrest were determined with real-time PCR and western blot. The cytotoxic effect of OHF on AGS cells was observed in a dose-dependent manner. Exposure to OHF ($100{\mu}g/mL$) significantly induced (P<0.05) the G1 phase cell cycle arrest. Additionally, the apoptotic cell population was greater (P<0.05) in OHF ($200{\mu}g/mL$) treated AGS cells when compared to the control. The expression of genes associated with cell cycle progression (Cdk4, Cdk2, and cyclin E) was significantly downregulated (P<0.05) by the OHF treatment. Moreover, the expression of Bax and caspase-3 in OHF treated cells was higher (P<0.05) than in the control. These findings suggest that OHF induces the G1 phase cell cycle arrest and activation of mitochondria-mediated apoptosis pathway in AGS human gastric cancer cells.

• Nutrition Research and Practice
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• 제15권6호
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• pp.673-685
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• 2021

BACKGROUND/OBJECTIVES: Obesity is associated with the impaired regulation of T cells characterized by increased numbers of Th1 and Th17 cells and the dysregulation of vitamin D metabolism. Both obesity and vitamin D have been reported to affect autophagy; however, a limited number of studies have investigated the effects of vitamin D on T cell autophagy in obese mice. Therefore, we aimed to determine whether in vitro treatment with vitamin D affects the proliferation, function, and autophagy of T cells from obese and control mice. MATERIALS/METHODS: Five-week-old male C57BL/6 mice were fed control or high-fat diets (10% or 45% kcal fat: CON or HFDs, respectively) for 12 weeks. Purified T cells were stimulated with anti-CD3 and anti-CD28 monoclonal antibodies and cultured with either 10 nM 1,25(OH)₂D₃ or 0.1% ethanol (vehicle control). The proliferative response; expression of CD25, Foxp3, RORγt, and autophagy-related proteins (LC3A/B, SQSTM1/P62, BECLIN-1, ATG12); and the production of interferon (IFN)-γ, interleukin (IL)-4, IL-17A, and IL-10 by T cells were measured. RESULTS: Compared with the CON group, T cell proliferation tended to be lower, and the production of IFN-γ was higher in the HFD group. IL-17A production was reduced by 1,25(OH)2D₃ treatment in both groups. The LC3 II/I ratio was higher in the HFD group than the CON group, but P62 did not differ. We observed no effect of vitamin D treatment on T cell autophagy. CONCLUSIONS: Our findings suggest that diet-induced obesity may impair the function and inhibit autophagy of T cells, possibly leading to the dysregulation of T cell homeostasis, which may be behind the aggravation of inflammation commonly observed in obesity.

• Preventive Nutrition and Food Science
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• 제7권3호
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• pp.250-254
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• 2002

The anticancer effects of leek (buchu in Korean) kimchi were evaluated in the human cancer cells: AGS gastric adenocarcinoma cells, HT-29 human colon adenocarcinoma cells and HL-60 leukemia cells. The leek kimchi (fermented for 6 days at 15$^{\circ}C$) was fractionated into 7 groups: methanol extract, hexane extract, methanol soluble extract MSE), dichloromethane (DCM) fraction (fr.), ethyl acetate fr., butanol fr. and aqueous fr. Most of the leek kimchi tractions inhibited the growth of AGS and HT-29 cancer cells in a dose dependent manner. In particular, the DCM fr. showed the highest inhibitory effect among the tractions. Treatment with the DCM fr. (0.1 mg/mL) reduced the survival rates of AGS and HT-29 cancer cells to 19% and 37% of the controls, respectively. Moreover the DCM fr. of the leek kimchi arrested G2/M phase in the cell cycle and induced apoptosis in HL-60 human promyelocytic leukemia cells. These results indicate that the leek kimchi exerted an anticancer effect on those human cancer cells, and that the DCM fr. arrested G2/M phase in the cell cycle and induced apoptosis in the leukemia cells.

• 한국식품영양학회지
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• 제9권1호
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• pp.92-98
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• 1996

Pectic materials, which are widely spread in the plant cell wall as plant carbohydrates, plays a great role in food Industry that acts as a softening agent of fruits and vegetables, and gel forming agents. To study physiochemical properties and industrial applications of pectic enzymes that hydrolyzes pectin, classification, assay method and Industrial application are reviewed based on previous results.

• Nutrition Research and Practice
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• 제15권3호
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• pp.294-308
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• 2021

BACKGROUD/OBJECTIVES: Allomyrina dichotoma larva (ADL), one of the many edible insects recognized as future food resources, has a range of pharmacological activities. In a previous study, an ADL extract (ADLE) reduced the hepatic insulin resistance of high-fat diet (HFD)-induced diabetic mice. On the other hand, the associated molecular mechanisms underlying pancreatic beta-cell dysfunction remain unclear. This study examined the effects of ADLE on palmitate-induced lipotoxicity in a beta cell line of a rat origin, INS-1 cells. MATERIALS/METHODS: ADLE was administered to high-fat diet treated mice. The expression of apoptosis-related molecules was measured by Western blotting, and reactive oxidative stress generation and nitric oxide production were measured by DCH-DA fluorescence and a Griess assay, respectively. RESULTS: The administration of ADLE to HFD-induced diabetic mice reduced the hyperplasia, 4-hydroxynonenal levels, and the number of apoptotic cells while improving the insulin levels compared to the HFD group. Treatment of INS-1 cells with palmitate reduced insulin secretion, which was attenuated by the ADLE treatment. Furthermore, the ADLE treatment prevented palmitate-induced cell death in INS-1 cells and isolated islets by reducing the apoptotic signaling molecules, including cleaved caspase-3 and PARP, and the Bax/Bcl2 ratio. ADLE also reduced the levels of reactive oxygen species generation, lipid accumulation, and nitrite production in palmitate-treated INS-1 cells while increasing the ATP levels. This effect corresponded to the decreased expression of inducible nitric oxide synthase (iNOS) mRNA and protein. CONCLUSIONS: ADLE helps prevent lipotoxic beta-cell death in INS-1 cells and HFD-diabetic mice, suggesting that ADLE can be used to prevent or treat beta-cell damage in glucose intolerance during the development of diabetes.

• 한국축산식품학회지
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• 제39권3호
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• pp.371-378
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• 2019

The objective of this study was to develop mathematical models for describing the kinetic behavior of Staphylococcus aureus (S. aureus) in seasoned beef jerky. Seasoned beef jerky was cut into 10-g pieces. Next, 0.1 mL of S. aureus ATCC13565 was inoculated into the samples to obtain 3 Log CFU/g, and the samples were stored aerobically at $10^{\circ}C$, $20^{\circ}C$, $25^{\circ}C$, $30^{\circ}C$, and $35^{\circ}C$ for 600 h. S. aureus cell counts were enumerated on Baird Parker agar during storage. To develop a primary model, the Weibull model was fitted to the cell count data to calculate Delta (required time for the first decimal reduction) and ${\rho}$ (shape of curves). For secondary modeling, a polynomial model was fitted to the Delta values as a function of storage temperature. To evaluate the accuracy of the model prediction, the root mean square error (RMSE) was calculated by comparing the predicted data with the observed data. The surviving S. aureus cell counts were decreased at all storage temperatures. The Delta values were longer at $10^{\circ}C$, $20^{\circ}C$, and $25^{\circ}C$ than at $30^{\circ}C$ and $35^{\circ}C$. The secondary model well-described the temperature effect on Delta with an $R^2$ value of 0.920. In validation analysis, RMSE values of 0.325 suggested that the model performance was appropriate. S. aureus in beef jerky survives for a long period at low storage temperatures and that the model developed in this study is useful for describing the kinetic behavior of S. aureus in seasoned beef jerky.

• Journal of Nutrition and Health
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• 제32권3호
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• pp.318-326
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• 1999

Apoptotic cell death, characterized by DNA fragmentation and morphological changes, has previously been shown to occur in vascular endothelial cells cultured with hydrogen peroxide. The present study examined the induction of apoptosis by hydrogen peroxide and whether pyruvate, a key glycolytic intermediate and $\alpha$-keto-monocarboxylate, can inhibit the apoptotic effects in bovine pulmonary artery endothelial cells(BPAECs). Culture with 500uM hydrogen peroxide resulted in 30% cell death and induced morphological changes and DNA fragmentation. Cell injury was inhibited by the treatment with pyruvate. Pyruvate(0.1-5.0mM), and cell viability increased in a dose-dependent manner. In the presence of pyruvate(10~20mM), the viability was improved to over 95%. In contrast, treatment with lactate, a reduced form of phyuvate, did not protect against cell death oxidative stress-induced loss of viability and apoptosis was examined with $\alpha$-cyano-3-hydroxycinnarmate(COHC) as a selective mitochondrial monocarboxylate transport blocker. Incubation with COHC(500uM) did not significantly affect cell viability in the presence of hydrogen peroxide. The cytoprotection by pyruvate(3mM)against hydrogen peroxide stress was abolished by COHC. This indicates that the cytoprotection by pyruvate against oxidative stress in endothelial cells is mediated, at least in part, by mitochondrial pyruvate uptake and hence endothelial enerygetics. However, cytosolic mechanisms related, at least in part, by mitochondrial pyruvate uptake and hence endothelial energetics. However, cytosolic mechanisms related to the glutathione system may also contribute. The results suggest that pyruvate has therapeutic potential in the treatment of oxidative stress-induced cytotoxicity associated with increased apoptosis.