• Journal of the Korean Society of Food Science and Nutrition
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• v.45 no.6
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• pp.805-811
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• 2016

This study was conducted to investigate the protective effects of water extract from Crassostrea gigas (CGW) against ethanol-induced hepatic toxicity in rats. Seventy-two male Wistar rats (6-week-old) were divided into six groups of 12 animals each: control group (1 mL saline/d), ethanol-treated group, positive control group (ethanol+Hovenia dulcis Thunb extract), CGWL group (ethanol+low dosage of CGW), CGWM group (ethanol+medium dosage of CGW), and CGWH group (ethanol+high dosage of CGW). All groups except the control group received ethanol (40% ethanol 5 g/kg) orally. CGW administration with ethanol resulted in prevention of ethanol-induced hepatotoxicity by increasing levels of serum alanine aminotransferase and ${\gamma}-glutamyltransferase$. CGW supplementation significantly reduced formation of malonaldehyde and inhibited reduction of hepatic glutathione and peroxidase levels, as compared with the ethanol-administration group. Further, CGW suppressed expression of CYP2E1, which was elevated by ethanol administration. Consequently, our results indicate that Crassostrea gigas may exert hepatoprotective effects against alcohol-induced hepatocyte injury by intensifying the anti-oxidative defense system.

• Preventive Nutrition and Food Science
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• v.9 no.1
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• pp.53-57
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• 2004

The purpose of this study was to investigate the effects of green tea catechin on mixed function oxidase system (MFO), lipofuscin contents, carbonyl value, oxidative damage and the antioxidative defense system in lung of microwave exposed rats. Experimental groups were divided to normal group and microwave exposed group. The microwave exposed groups were subdivided into three groups: catechin free diet (MW-0C) group, 0.25% catechin (MW-0.25C) group and 0.5 ％ catechin (MW-0.5C) group according to the levels of dietary catechin supplementation. The rats were irradiated with microwave at frequency of 2.45 GHz for 15 min. Experimental animals were sacrificed at 6th day after microwave irradiation. The contents of cytochrome P$_{450}$ contents in MW-0C group was increased to 95% , compared with normal group. MW-0.25C and MW-0.5C groups were reduced to 16% and 31%, respectively, compared with MW-0C group. The activity of NADPH-cytochrome P$_{450}$ reductase in MW-0C group was increased to 44%, compared with normal group. MW-0.25C and MW-0.5C groups were reduced to 12% and 17％, respectively, compared with MW-0C group. The activity of superoxide dismutase (SOD) in MW-0C group was decreased to 21 ％, compared with normal group. MW-0.25C and MW-0.5C group were significantly (p < 0.05) increased, compared with MW-0C group. The activity of glutathione peroxidase (GSHpx) in MW-0C group was significantly decreased, compared with normal group. MW-0.25C and MW-0.5C groups were recovered to the level of normal group. The thiobarbituric acid reactive substances (TBARS) content in MW-0C group was increased to 34 ％, compared with normal group. Catechin supplementation groups were maintained the level of normal group. The levels of caybonyl value in MW-0C group was increased to 21 ％, compared with normal group. MW-0.25C and MW-0.5C groups were reduced to 14% and 12%, respectively, compared with MW-0C group. The lipofuscin contents in MW-0C group were increased to 23.4 ％, compared with normal group. That of MW-0.5C group was significantly reduced, compared with MW-0C group. In conclusion, MFO system was activated and the formation of oxidized protein, lipofuscin was increased and antioxidative defense system was weakened of lung tissue in microwave exposed rats, thus oxidative damage was increased. But it was rapidly recovered to normal level by green tea catechin supplementation.n.

• Journal of the Korean Society of Food Science and Nutrition
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• v.44 no.5
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• pp.649-656
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• 2015

The protective effect of zinc against cortisol-induced cell injury was examined in rainbow trout gill epithelial cells. Cells exposed to cortisol for 24 h showed increased leakage of lactate dehydrogenase (LDH) as well as decreased cell viability in a dose-dependent manner. Treatment with zinc ($100{\mu}M$ $ZnSO_4$) reduced the severity of both LDH release and cell death as well as protected cells against cortisol-induced caspase-3 activation, indicating reduction of apoptosis. Cortisol-induced cell death, leakage of LDH, and caspase-3 activation were blocked by the glucocorticoid receptor antagonist Mifepristone (RU-486), suggesting that cell injury was cortisol-dependent. In addition, we studied the effect of zinc on the expression of antioxidant genes such as metallothionein A (MTA), metallothionein B (MTB), glutathione-S-transferase (GST), and glucose-6-phosphate dehydrogenase (G6PD) during cortisol-induced cell injury. MTA, MTB, GST, and G6PD mRNA levels increased after treatment with zinc or cortisol, separately or in combination. Higher mRNA levels of MTA, MTB, GST, and G6PD were detected when cells were treated with $100{\mu}M$ $ZnSO_4$ and $1{\mu}M$ cortisol in combination at the same time compared to treatment with zinc or cortisol separately. Cells treated with zinc showed increased intracellular free zinc concentrations, and this response was significantly enhanced in cells treated with cortisol and zinc. In conclusion, zinc treatment inhibited cortisol-induced cytotoxicity and apoptosis through indirect antioxidant action.

• Korean Journal of Food Science and Technology
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• v.47 no.3
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• pp.388-393
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• 2015

This study aimed to investigate the therapeutic effect of rutin against whole-body ${\gamma}$-irradiation in BALB/c mice. BALB/c mice were randomly divided into four groups and exposed to 6 Gy ${\gamma}$-irradiation. One hour later, mice were orally administered rutin (50 and 100 mg/kg) for seven consecutive days. ${\gamma}$-Irradiation (6 Gy) resulted in cellular damage as manifested by elevated levels of plasma hepatic marker enzymes and lipid peroxidation in liver tissue, accompanied with decreased spleen and thymus indices, and white blood cell count. In addition, ${\gamma}$-irradiation significantly decreased the levels of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase and catalase. Rutin treatment significantly protected against ${\gamma}$-irradiation-induced cellular damage, which was evident by the improvement in the status of most of the investigated parameters. Therefore, rutin has beneficial effects against radiation-induced damage.

• Journal of Life Science
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• v.27 no.7
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• pp.826-833
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• 2017

The rising concentration of atmospheric carbon dioxide is causing ocean acidification and global warming. The seahorse is an important species in marine ecosystems and fishery markets, however, their populations have recently decreased due to ocean acidification. As a result, we examined changes in the physiological responses of the spotted seahorse Hippocampus kuda when it was exposed to acidic sea water (pH 6.0, 6.5, and 7.0) and normal seawater (pH 8.0 as the control) over a period of 15 days. As the pH decreased, the seahorses' body weight and length also decreased. Components in body of ash, the crude lipids and crude proteins also differed significantly with changes in pH, due to stress caused by the seahorses' exposure to the acidic water conditions. The superoxide dismutase levels were significantly lower in the pH 6.0 and 6.5 groups than they were in the pH 7.0 and pH 8.0 groups. However, the catalase and glutathione levels were significantly higher in the acidic sea water groups. We suggest that decreasing the pH level of rearing water induces a stress response in H. kuda, damaging their ability to maintain their homeostasis and energy metabolism. Antioxidant enzymes are generally sensitive to acidic stress; in this study, the antioxidant activity was significantly affected by the pH level of the rearing water. These results indicate that physiological stress, induced by exposure to acidification, induces an antioxidant reaction, which can reduce general components in the body and the growth of H. kuda.

• Journal of Veterinary Clinics
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• v.29 no.5
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• pp.372-376
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• 2012

Acute kidney injury (AKI) is a serious problem associated with high morbidity and mortality. Ischemia-reperfusion is an important cause of acute kidney injury. This study was performed to ascertain clinically useful biomarkers for the diagnosis of AKI. In three miniature pigs, AKI were induced by 60 minutes of bilateral renal ischemia by the clamping renal artery. Blood and urine samples were collected from the pigs prior to clamping (baseline) and 0, 1, 3 and 5 days post-clamping. Serum blood urea nitrogen (BUN), creatinine, sodium and uric acid were measured in serum and urine samples. Fractional excretion of sodium ($FE_{Na}$) and fractional excretion of uric acid ($FE_{UA}$) were calculated. Also, interleukin (IL)-6, IL-18, liver type fatty acid binding protein (L-FABP) and glutathione-S-transferase (GST) were detected by Western immunoblotting. Serum BUN and creatinine levels were increased significantly at day 1 post-clamping in all three miniature pigs. However, $FE_{Na}$ and $FE_{UA}$ showed marked individual differences. Western immunoblotting revealed significantly increased levels of IL-6, IL-18, L-FABP and GST in post-ischemic urine, compared to pre-clamping. While more research concerning the variance of $FE_{Na}$ and $FE_{UA}$ is needed, serum BUN, creatinine, IL-6, IL-18, L-FABP and GST may be sensitive urine biomarkers for diagnosis of AKI together with other biomarkers in the porcine ischemia-reperfusion model.

• Korean Journal of Medicinal Crop Science
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• v.15 no.6
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• pp.437-443
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• 2007

This study was carried out to investigate the effect of dietary supplementation with red ginseng water-extracts on the induction of microsomal cytochrome P-450 in rats. Phenobarbital (PB) and 3-methylcholanthrene (3-MC), P-450 inducers, were administered to 3- or 12-month old rats received red ginseng extracts (25 mg/kg) from 6 weeks to 12 months for 3 days. PB and 3-MC increased levels of P-450, P-450 reductase, ethoxycoumarin O-deethylase, benzphetamine N-demethylase and glutathione-S-transferase in the liver of rats. However, chronic administration of red ginseng significantly reduced these increase of enzyme levels induced by P-450 inducers. Chronic administration of red ginseng did not affect the induction of cytochrome $b_5$ and NADH cytochrome $b_5$ reductase by P-450 inducers. It is suggested that the induction of cytochrome P-450 system in the liver in relation to xenobiotics toxicity can be modulated by long-term supplementation with Korean red ginseng to rats.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.11
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• pp.1286-1292
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• 2017

This study was conducted to investigate the hepatoprotective effects of 3,5-dicaffeoylquinic acid (3,5-DCQA) isolated from Ligularia fischeri against hydrogen peroxide-induced oxidative stress in HepG2 cells. Antioxidative effects of 3,5-DCQA were determined by measuring antioxidant enzyme [superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx)] expression levels against hydrogen peroxide-induced oxidative stress using real-time PCR analysis. 3,5-DCQA treatment significantly increased gene expression levels of SOD, CAT, and GPx in a dose-dependent manner ($10{\sim}30{\mu}g/mL$) in HepG2 cells. Hepatoprotective effects were analyzed by measuring glutamic oxaloacetic transaminase (GOT), lactate dehydrogenase (LDH), and gamma-glutamyl transferase (GGT) activities using a biochemistry analyzer in hydrogen peroxide-treated HepG2 cells. 3,5-DCQA treatment significantly reduced GOT, LDH, and GGT activities in a dose-dependent manner ($10{\sim}30{\mu}g/mL$) against increased liver function index enzyme activities induced by hydrogen peroxide oxidative stress in HepG2 cells. The results reveal that 3,5-DCQA compound isolated from Ligularia fischeri can be useful for the development of an effective hepatoprotective agent.

• Journal of the Korean Society of Food Science and Nutrition
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• v.26 no.4
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• pp.675-681
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• 1997

This study was conducted to investigate the effect of dietary protein and fiber levels on the activities of ethanol metabolizing enzymes of liver in ethanol-treated rats. Sprague-Dawley male rats were fed on diets containing two levels of protein(7, 20%/kg diet) and pectin(5, 10%/kg diet). In ethanol experiments, ethanol(25% v/v) was administered by oral intubation(5g/kg body weight) at the same time once a day Control animals received an isocaloric dose of sucrose. The rats were sacrificed after 5 weeks of feeding periods. Alcohol dehydrogenase and microsomal ethanol oxidizing system activities of hepatic tissue were increased more in ethanol-treated groups than in control groups. Increment of activities predominated in normal protein normal fiber group. Aldehyde dehydrogenase activity was decreased in ethanol-treated groups and significantly decreased in normal Protein normal fiber group. Cytochrome P-450 content was significantly increased in ethanol-treated groups and Predominated in normal protein groups. Xanthine oxidase activity was increased in ethanol-treated groups, but not significantly except normal protein normal fiber group. Glutathione content tended to increase in proportion to level of dietary protein and was higher in normal fiber groups than in high fiber groups, whereas it was decreased by ethanol treatment. Lipid Peroxide content was significantly increased in low Protein normal fiber groups.

• IMMUNE NETWORK
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• v.23 no.6
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• pp.48.1-48.21
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• 2023

Mesenchymal stromal/stem cells (MSCs) possess immunoregulatory properties and their regulatory functions represent a potential therapy for acute lung injury (ALI). However, uncertainties remain with respect to defining MSCs-derived immunomodulatory pathways. Therefore, this study aimed to investigate the mechanism underlying the enhanced effect of human recombinant bone morphogenic protein-2 (rhBMP-2) primed ES-MSCs (MSC^BMP2) in promoting Tregs in ALI mice. MSC were preconditioned with 100 ng/ml rhBMP-2 for 24 h, and then administrated to mice by intravenous injection after intratracheal injection of 1 mg/kg LPS. Treating MSCs with rhBMP-2 significantly increased cellular proliferation and migration, and cytokines array reveled that cytokines release by MSC^BMP2 were associated with migration and growth. MSC^BMP2 ameliorated LPS induced lung injury and reduced myeloperoxidase activity and permeability in mice exposed to LPS. Levels of inducible nitric oxide synthase were decreased while levels of total glutathione and superoxide dismutase activity were further increased via inhibition of phosphorylated STAT1 in ALI mice treated with MSC^BMP2. MSC^BMP2 treatment increased the protein level of IDO1, indicating an increase in Treg cells, and Foxp3⁺CD25⁺ Treg of CD4⁺ cells were further increased in ALI mice treated with MSC^BMP2. In co-culture assays with MSCs and RAW264.7 cells, the protein level of IDO1 was further induced in MSC^BMP2. Additionally, cytokine release of IL-10 was enhanced while both IL-6 and TNF-α were further inhibited. In conclusion, these findings suggest that MSC^BMP2 has therapeutic potential to reduce massive inflammation of respiratory diseases by promoting Treg cells.