• Journal of Nutrition and Health
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• v.55 no.3
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• pp.348-358
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• 2022

Purpose: Hyperglycemia accelerates the formation of advanced glycation end products (AGEs), a group of compounds formed via non-enzymatic glycation/glycoxidation. Type 2 diabetes mellitus (T2DM) is related to oxidative stress, resulting in some overgeneration of AGEs. The accumulation of AGEs in T2DM patients leads to increased inflammation, DNA damage, tissue damage, progression of diabetic microvascular disease, and nephropathy. Heme oxygenase-1 (HO-1) is an intracellular enzyme that catalyzes the oxidation of heme. Expression of HO-1 in the endothelium and in muscle monocytes/macrophages was upregulated upon exposure to reactive oxygen species or oxidized low-density lipoprotein. Cells activated by oxidative stress are reported to release HO-1 in the serum. In the current study, we discuss the oxidative status according to the level of AGEs and the association of HO-1 with AGEs or urinary DNA damage marker in type 2 diabetic Korean patients. Methods: This study enrolled 36 diabetic patients. Subjects were classified into two groups by serum AGEs level (Low AGEs group: < 0.85 ng/mL serum AGEs; High AGEs group: ≥ 0.85 ng/mL serum AGEs). Body composition was measured using bioelectrical impedance analysis. Blood and urinary parameters were measured using commercial kits. Results: No significant differences were observed in the general characteristics and body composition between the two groups. Serum HO-1 concentration was significantly higher in the High AGEs group than in the Low AGEs group. After adjustment of age and gender, a correlation was performed to assess the association between serum HO-1 and serum AGEs or urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG). Our results indicate that serum HO-1 is positively correlated with serum AGEs and urinary 8-OHdG. Conclusion: Taken together, our results indicate that in diabetes patients, a high level of HO-1 is associated with a high concentration of AGEs and 8-OHdG, probably reflecting a protective response against oxidative stress.

• Korean Journal of Exercise Nutrition
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• v.24 no.2
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• pp.30-37
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• 2020

[Purpose] The present study investigated the effect of endurance exercise with blood flow restriction (BFR) performed at either 25% maximal oxygen uptake (${\dot{V}}O_2$ max) or 40% ${\dot{V}}O_2$ max) on muscle oxygenation, energy metabolism, and endocrine responses. [Methods] Ten males were recruited in the present study. The subjects performed three trials: (1) endurance exercise at 40% ${\dot{V}}O_2$ max without BFR (NBFR40), (2) endurance exercise at 25% ${\dot{V}}O_2$ max with BFR (BFR25), and (3) endurance exercise at 40% ${\dot{V}}O_2$ max with BFR (BFR40). The exercises were performed for 15 min during which the pedaling frequency was set at 70 rpm. In BFR25 and BFR40, 2 min of pressure phase (equivalent to 160 mmHg) followed by 1 min of release phase were repeated five times (5 × 3 min) throughout 15 minutes of exercise. During exercise, muscle oxygenation and concentration of respiratory gases were measured. The blood samples were collected before exercise, immediately after 15 min of exercise, and at 15, 30, and 60 minutes after completion of exercise. [Results] Deoxygenated hemoglobin (deoxy-Hb) level during exercise was significantly higher with BFR25 and BFR40 than that with NBFR40. BFR40 showed significantly higher total-hemoglobin (total-Hb) than NBFR40 during 2 min of pressure phase. Moreover, exercise-induced lactate elevation and pH reduction were significantly augmented in BFR40, with concomitant increase in serum cortisol concentration after exercise. Carbohydrate (CHO) oxidation was significantly higher with BFR40 than that with NBFR40 and BFR25, whereas fat oxidation was lower with BFR40. [Conclusion] Deoxy-Hb and total Hb levels were significantly increased during 15 min of pedaling exercise in BFR25 and BFR40, indicating augmented local hypoxia and blood volume (blood perfusion) in the muscle. Moreover, low-and moderate-intensity exercise with BFR facilitated CHO oxidation.

• Journal of Ginseng Research
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• v.47 no.3
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• pp.366-375
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• 2023

Background: Ginseng contains three active components: ginsenosides, gintonin, and polysaccharides. After the separation of 1 of the 3 ingredient fractions, other fractions are usually discarded as waste. In this study, we developed a simple and effective method, called the ginpolin protocol, to separate gintonin-enriched fraction (GEF), ginseng polysaccharide fraction (GPF), and crude ginseng saponin fraction (cGSF). Methods: Dried ginseng (1 kg) was extracted using 70% ethanol (EtOH). The extract was water fractionated to obtain a water-insoluble precipitate (GEF). The upper layer after GEF separation was precipitated with 80% EtOH for GPF preparation, and the remaining upper layer was vacuum dried to obtain cGSF. Results: The yields of GEF, GPF, and cGSF were 14.8, 54.2, and 185.3 g, respectively, from 333 g EtOH extract. We quantified the active ingredients of 3 fractions: L-arginine, galacturonic acid, ginsenosides, glucuronic acid, lysophosphatidic acid (LPA), phosphatidic acid (PA), and polyphenols. The order of the LPA, PA, and polyphenol content was GEF > cGSF > GPF. The order of L-arginine and galacturonic acid was GPF >> GEF = cGSF. Interestingly, GEF contained a high amount of ginsenoside Rb1, whereas cGSF contained more ginsenoside Rg1. GEF and cGSF, but not GPF, induced intracellular [Ca²⁺]_i transient with antiplatelet activity. The order of antioxidant activity was GPF > GEF = cGSF. Immunological activities (related to nitric oxide production, phagocytosis, and IL-6 and TNF-α release) were, in order, GPF > GEF = cGSF. The neuroprotective ability (against reactive oxygen species) order was GEF > cGSP > GPF. Conclusion: We developed a novel ginpolin protocol to isolate 3 fractions in batches and determined that each fraction has distinct biological effects.

• Exercise Science
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• v.21 no.1
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• pp.111-120
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• 2012

The purpose of the study was to assess the effects of different cardiorespiratory fitness response to exercise training on cardiovascular disease and adipocytokine release and gene expression in abdominal obesity women. forty eight middle-age women were divided to a exercise-responder (n=34) group (ERG) and a exercise-nonresponder (n=14) group (ENRG) based on cardiorespiratory fitness after exercise training (12weeks, 1200 kcal/week, moderate-vigorous intensity, walking and jogging). Cardiorespiratory fitness was measured using maximal oxygen uptake with metabolic gas analysis and body composition was determined by bioelectrical impedance. We measured lipid and glucose profiles, blood adipocytokines and adipocytokine genes expression in adipose tissue. Waist girth (p=0.040), and %body fat (p=0.031) were significantly decreased in ERG than ENRG. Triglyceride (p=0.023) and systolic blood pressure (0.046) were significantly decreased in ERG than ENRG. Blood leptin (p=0.022) was significantly decrease in ERG than ENRG but leptin gene expression was decreased both groups (p<0.001). These results show that exercise-responder group improved cardiovascular disease risk factors and adipocytokine more than exercise-nonresponder group after exercise training. Moreover, exercise-nonresponders group show that obese indices and blood leptin and leptin gene expression in adipose tissue were decreased despite the failure to improve fitness. Therefore, regular exercise training seems to give health benefits although the failure to improve fitness.

• Journal of Food Hygiene and Safety
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• v.39 no.3
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• pp.273-280
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• 2024

In this study, the antibacterial activity and mechanisms of bitter orange extract, a natural antibacterial agent, were investigated, with a focus on its potential application in washing water for controlling Salmonella Typhimurium contamination of salad, a ready-to-eat food. The minimum inhibitory concentration (MIC) of bitter orange extract against S. Typhimurium was determined using the broth dilution method. Subsequently, S. Typhimurium was exposed to various concentrations of bitter orange extract (1/16 MIC-2 MIC) and growth curves were measured. Following treatment with bitter orange extract, we investigated its antibacterial mechanism by measuring intracellular reactive oxygen species (ROS) levels, alterations in membrane potential and integrity, and nucleic acid leakage in S. Typhimurium. Additionally, salads artificially contaminated with S. Typhimurium were treated with different concentrations of bitter orange extract using the dipping method for various durations to assess the reduction effect. The MIC of bitter orange extract against S. Typhimurium was 195.313 mg/L, and bacterial growth was completely inhibited at a concentration of 1 MIC. Furthermore, an increase in bitter orange extract concentration correlated with elevated intracellular ROS levels, membrane potential disruption, membrane damage, and nucleic acid release. Importantly, salads treated with bitter orange extract exhibited a significant reduction in S. Typhimurium counts compared to the control, and prolonged treatment times resulted in further reductions in bacterial counts. Bitter orange extract was more effective than sodium hypochlorite and can be used as a safer salad wash. These findings indicate the potential treatment of salads to prevent foodborne illnesses.

• Food Science and Preservation
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• v.18 no.1
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• pp.124-129
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• 2011

PC12 neuronal cell-protective effects of hot water extracts of guava fruit and leaf were evaluated. Total phenolic levels in fruit and leaf were 11.75 and 293.25 mg/g, respectively. Gallic acid, the predominant phenoic, was detected in both extracts. Intracellular reactive oxygen species (ROS) accumulation after $H_2O_2$ treatment was significantly reduced when the hot water extract of guava leaf was added to cell medium, compared to PC12 cells treated with $H_2O_2$ only. In a cell viability assay using 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyl- tetrazoliumbromide (MTT), the hot water extracts of fruit and leaf protected against $H_2O_2$-induced neurotoxicity. The leaf extract was more effective in terms of inhibition of lactate dehydrogenase (LDH) release into medium, compared to the fruit extract. These in vitro data suggest that hot water extracts of guava fruit and leaf may be useful in treatment of neurodegenerative conditions such as Alzheimer's disease.

• Journal of the korean academy of Pediatric Dentistry
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• v.33 no.1
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• pp.13-24
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• 2006

Neuronal apoptotic events, consequently resulting in neuronal cell death, are occurred in hypoxic/ischemic condition. This cell death has been shown to be accompanied with the production of reactive oxygen species (ROS), which can attack cellular components such as nucleic acids, proteins and phospholipid. However, the underlying mechanisms of apoptosis induced in hypoxic/ischemic condition and its treatment methods are unsettled. Cobalt chloride $(CoCl_2)$ has been known to mimic hypoxic condition including the production of ROS. Epigallocatechin gallate (EGCG), a green tea polyphenol, has diverse pharmacologial activities in cell growth and death. This study was aimed to investigate the apoptotic mechanism by $CoCL_2$ and effects of EGCG on $CoCl_2-induced$ apoptosis in PC12 cells. Administration of $CoCl_2$ decreased cell survival in dose- and time-dependent manners and induced genomic DNA fragmentation. Treatment with $100{\mu}M$ EGCG for 30 min before PC12 cells were exposed to $150{\mu}M$ $CoCl_2$, being resulted in the cell viability and DNA fragmentation being rescued. $CoCl_2$ caused morphologic changes such as cell swelling and condensed nuclei whereas EGCG attenuated morphologic changes by $CoCl_2$. EGCG suppressed the apoptotic peak and a loss of ${\Delta}{\psi}_m$ induced by $CoCl_2$. $CoCl_2$ decreased Bcl-2 expression but Bax expression was not changed in $CoCl_2$- treated cells. EGCG attenuated the Bcl-2 underexpression by $CoCl_2$. $CoCl_2$ augumented the cytochrome c release from mitochondria into cytoplasm and increased caspase-8, -9 and caspase-3 activity a marker of the apoptotic executing stage. EGCG ameliorated the incruement in caspase-8, -9 and -3 activity, and cytochrome c release by $CoCl_2$ NAC (N-acetyl-cysteine), a scavenger of ROS, attenuated $CoCl_2-induced$ apoptosis in consistent with those of EGCG. These results suggest that $CoCl_2$ induces apoptotic cell death through both mitochondria- and death receptor-dependent pathway and EGCG has neuroprotective effects against $CoCl_2-induced$ apoptosis in PC12 cells.

• Journal of Life Science
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• v.29 no.5
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• pp.555-563
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• 2019

This study was undertaken to investigate the effect of an ethanol extract of Elaeagnus umbellata leaves (EUL-EE) on skin-related biological activities. Previously, we have reported that gallic acid was the major phenolic compound in EUL-EE through quantitative analysis and that EUL-EE had an inhibitory effect against the proliferation of liver cancer HepG2 cells. In the present study, the inhibitory effects of EUL-EE on melanin production and tyrosinase activity in ${\alpha}$-melanocyte-stimulated hormone-stimulated B16-F0 cells were determined to assess the effects of EUL-EE on skin whitening. The anti-wrinkle effect using UVB-irradiated CCD-986sk cells was examined by the expression of type I procollagen and metalloproteinase (MMP)-1 release. The EUL-EE significantly decreased intracellular melanin production (33.0% inhibition at $100{\mu}g/ml$) when compared with untreated B16-F0 cells. Tyrosinase activities in the stimulated B16-F0 cells were also decreased by EUL-EE (47.8% inhibition at $100{\mu}g/ml$). The EUL-EE also dose-dependently increased the production of type I procollagen (up to 1.74-fold at $250{\mu}g/ml$) in CCD-986sk cells when compared with UVB-irradiated controls. EUL-EE showed no cytotoxicity at concentrations up to $500{\mu}g/ml$. In addition, EUL-EE at $10-500{\mu}g/ml$ inhibited the release of MMP-1 to the medium from UVB-irradiated CCD-986sk cells. Taken together, these observations indicate that EUL-EE has high potential for use as inner beauty and cosmetic materials due to its whitening and anti-wrinkle effects.

• Journal of Environmental Impact Assessment
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• v.30 no.5
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• pp.271-296
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• 2021

Since the thermal stratification in a reservoir inhibits the vertical mixing of the upper and lower layers and causes the formation of a hypoxia layer and the enhancement of nutrients release from the sediment, changes in the stratification structure of the reservoir according to future climate change are very important in terms of water quality and aquatic ecology management. This study was aimed to develop a data-driven inflow water temperature prediction model for Daecheong Reservoir (DR), and to predict future inflow water temperature and the stratification structure of DR considering future climate scenarios of Representative Concentration Pathways (RCP). The random forest (RF)regression model (NSE 0.97, RMSE 1.86℃, MAPE 9.45%) developed to predict the inflow temperature of DR adequately reproduced the statistics and variability of the observed water temperature. Future meteorological data for each RCP scenario predicted by the regional climate model (HadGEM3-RA) was input into RF model to predict the inflow water temperature, and a three-dimensional hydrodynamic model (AEM3D) was used to predict the change in the future (2018~2037, 2038~2057, 2058~2077, 2078~2097) stratification structure of DR due to climate change. As a result, the rates of increase in air temperature and inflow water temperature was 0.14~0.48℃/10year and 0.21~0.41℃/10year,respectively. As a result of seasonal analysis, in all scenarios except spring and winter in the RCP 2.6, the increase in inflow water temperature was statistically significant, and the increase rate was higher as the carbon reduction effort was weaker. The increase rate of the surface water temperature of the reservoir was in the range of 0.04~0.38℃/10year, and the stratification period was gradually increased in all scenarios. In particular, when the RCP 8.5 scenario is applied, the number of stratification days is expected to increase by about 24 days. These results were consistent with the results of previous studies that climate change strengthens the stratification intensity of lakes and reservoirs and prolonged the stratification period, and suggested that prolonged water temperature stratification could cause changes in the aquatic ecosystem, such as spatial expansion of the low-oxygen layer, an increase in sediment nutrient release, and changed in the dominant species of algae in the water body.

• Journal of Nutrition and Health
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• v.54 no.6
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• pp.618-630
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• 2021

Purpose: The ginger rhizome (Zingiber officinale) is widely cultivated as a spice for its aromatic and pungent components. One of its constituents, 6-hydroxydopamine (6-OHDA) is usually thought to cross the cell membrane through dopamine uptake transporters, and induce inhibition of mitochondrial respiration and the generation of intracellular reactive oxygen species (ROS). This study examines the neuroprotective effect and acetylcholinesterase (AChE) inhibitory activity of fermented ginger extracts (FGEs) on 6-OHDA induced toxicity in SH-SY5Y human neuroblastoma cells. Methods: Ginger was fermented using 2 species of Bacillus subtilis, with or without enzyme pretreatment. Each sample was extracted with 70% ethanol. Neurotoxicity was assessed by applying the EZ-Cytox cell viability assay and by measuring lactic dehydrogenase (LDH) release. Morphological changes of apoptotic cell nuclei were observed by Hoechst staining. Cell growth and apoptosis of SH-SY5Y cells were determined by Western blotting and enzyme activity analysis of caspase-3, and AChE enzymatic activity was determined by the colorimetric assay. Results: In terms of cell viability and LDH release, exposure to FGE showed neuroprotective activities against 6-OHDA stimulated stress in SH-SY5Y cells. Furthermore, FGE reduced the 6-OHDA-induced apoptosis, as determined by Hoechst staining. The occurrence of apoptosis in 6-OHDA treated cells was confirmed by determining the caspase-3 activity. Exposure to 6-OHDA resulted in increased caspase-3 activity of SH-SY5Y cells, as compared to the unexposed group. However, pre-treatment with FGE inhibited the activity of caspase-3. The neuroprotective effects of FGE were also found to be caspase-dependent, based on reduction of caspase-3 activity. Exposure to FGE also inhibited the activity of AChE induced by 6-OHDA, in a dose-dependent manner. Conclusion: Taken together, our results show that FGE exhibits a neuroprotective effect in 6-OHDA treated SH-SY5Y cells, thereby making it a potential novel agent for the prevention or treatment of neurodegenerative disease.