• Korean Journal of Veterinary Research
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• v.35 no.4
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• pp.699-712
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• 1995

The present study, to evaluate the effect of vitamin E on the oxidative stress in STZ-treated rat and BB rat, was investigated the biochemical enzyme activity in the serum, and malondialdehyde and carbonyl group in the RBC membrane, liver and microsomal fraction after vitamin E and/ or insulin treatment. Results obtained through the experiments were summarized as follows; 1. Effect of vitamin E and/or insulin treatment in STZ-treated rat 1) Lipid peroxidation level in RBC membrane, liver and microsomal fraction was significantly decreased in vi. tamin E and/or insulin treatment group, and especially more significantly decreased in vitamin E with insulin treated group. 2) Protein oxidation level in RBC membrane, liver and microsomal fraction was significantly decreased in vitamin E and/or insulin treatment group. And it was especially more significantly decreased in RBC membrane and liver of vitamin E with insulin treated group. 3) In the enzyme activity in the serum, the activity of AST and ALT was not altered in all experimental group. The increased ALP activity in STZ-treated group was significantly decreased in insulin treated group and vitamin E with insulin treated group. 4) Decreased level of albumin and creatinine after STZ treatment was significantly increased in vitamin E and/or insulin treated group. 5) Level of glucose, cholesterol and triacylglycerol in serum: Glucose level was not significantly different in vitamin E treated group compared to STZ control group. But it was significantly different in the insulin treated group and vitamin E with insulin treated group compared to STZ control group. The cholesterol content in the serum was significantly increased in STZ control group compared to normal control group. And except low dose vitamin E treatment group, it was significantly decreased in vitamin E and/or insulin treated group compared to STZ control group. The triacylglycerol content in the serum was significantly decreased in STZ control group and increased in high dose vitamin E treated group and vitamin E with insulin treated group. But it was not significantly different in low dose vitamin E treated group and insulin treated group compared to STZ control group. 2. Effect of vitamin E and/or insulin treatment in BB rat 1) Lipid peroxidation level in liver was decreased by vitamin E with insulin treatment compared to insulin treatment. But it was not different in microsomal fractions. 2) Protein oxidation level in liver and microsomal fraction was decreased by vitamin E with insulin treatment compared to insulin treatment only in microsomal fractions. These results suggest that the combination treatment of vitamin E and insulin could prevent the oxidative change of lipid and protein of the RBC membrane, liver and microsomal fraction in STZ-treated rats and BB rats.

• Food Science and Preservation
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• v.18 no.1
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• pp.65-71
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• 2011

We explored the effect of extracts of dried Platycodon grandiflorum on production of reactive oxygen species (ROS), glutathione (GSH) and nitric oxide (NO). To determine antioxidant activity in the presence of $H_2O_2$-induced oxidative stress, DCFH-DA (dichlorodihydrofluorescin diacetate) assay was employed. Acetone/methylene chloride (A+M) and methanolic (MeOH) extracts of P. grandiflorum reduced intracellular ROS levels. Of the various tested fractions, n-BuOH fraction showed the highest protective effect in terms of lipid peroxide production. Total GSH levels were measured after treatment of HT1080 cells with the A+M and MeOH extracts, and other solvent fractions, at various concentration. The A+M extacts and 85% (v/v) aqueous MeOH fraction significantly increased GSH levels (p<0.05). When lipopolysaccharide (LPS)-induced NO production was evaluated, all tested crude extracts, and fractions thereof, significantly reduced NO production (p<0.05), and the n-BuOH and 85% (v/v) aqueous MeOH fractions (at 0.05 mg/mL) showed the strongest inhibitory effects. The results showed that the n-BuOH fraction inhibited both cellular oxidation and NO production, and this fraction may thus contain valuable active compounds.

• Korean Journal of Materials Research
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• v.8 no.6
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• pp.505-512
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• 1998

In this study, two-layer thermal barrier coatings composed of plasma sprayed 0.3mm $ZrO_2(8wt% Y_2o_3)$ ceramic coating layer and O.lmm $NiCrAlCoY_20_3$ bond coating layer on AISI 316 were investigated microstructure of the coating, oxidation of the metallic bond coating and adhesive strength to evaluate the durability of coating layer after cyclic and isothermal test at 90$0^{\circ}C$. And quantitative phase analysis of $ZrO_2(8wt% Y_2o_3)$ ceramic coating was performed as a function of thermal exposure time using XRD technique. The results showed that the amount of m - 2rO, phase in the coating was slightly increased with increasing thermal exposure time at 90$0^{\circ}C$. The c/a ratio of t' - $ZrO_2$ in the as-sprayed coating was 1.0099 and slightly increased to 1.0115 after 100 hours heat treatment. It was believed that $Y_2O_3$ in high yttria tetragonaJ(t') was transformed to low yttria tetragonaJ(t) by $Y_2O_3$ diffusion with increasing thermal exposure time. The adhesive strength was gradually decreased as thermal exposure time increased. After the isothermal test, the failure predominantly occured in ceramic coating layer. On the other hand. the specimens after cyclic thermal test were mostly failed at bond coating/ceramic coating interface. The failure was oeeured by decreasing the bond strength between bond coating and oxide scale which were formed by oxidation of the metallic elements within bond coating and by thermal stress due to thermal expansion mismatches between the oxide scale and ceramic coating.

• Journal of the Korean Society of Food Science and Nutrition
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• v.33 no.6
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• pp.973-980
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• 2004

To evaluate the antioxidative effect of rice coated with maengjong-juk extract in vivo system, rice coated with maengjong-juk extract diets were fed to NZW rabbit for 16 weeks and lipid peroxidation, protein oxidation, activities of antioxidative enzymes and total glutathione content in tissues were measured. TBARS contents in liver and spleen were significantly decreased in maengjong-juk extract diet group compared to control group, while those in kidney and heart tissue were not significantly different. Maengjong-juk extract diet suppressed the protein oxidation significantly in liver, spleen, kidney and heart tissues. Hepatic total SOD, Cu$.$Zn-SOD and Mn-SOD activities of maengjong-juk extract diets were significantly higher than those of control diet. GSH-Px and catalase activities of maengjong-juk extract diet were higher than those of control, while GR activities show no significant difference between the two groups. Total hepatic glutathione content was significantly increased by maengjong-juk extract diet. According to this study, many antioxidative materials and phytochemicals in maengjong-juk extracts seems to protect tissues from oxidative stress by stimulating antioxidative systems in atherosclerotic rabbit fed high cholesterol diet.

• Journal of Korean Medicine Rehabilitation
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• v.29 no.2
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• pp.115-133
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• 2019

Objectives The purpose of this study was to evaluate the effects of Curcumae Longae Rhizoma pharmacopuncture on the monosodium iodoacetate (MIA)-induced osteoarthritis rats. Methods Osteoarthritis was induced by injection of MIA ($50{\mu}L$ with 80 mg/mL) into knee joint cavity of rats. Rats were divided into 6 groups. Normal group was injected by normal saline into knee joint cavity only. Control group was induced for osteoarthritis by MIA and orally administered with distilled water. Normal Saline group was induced for osteoarthritis by MIA and injected with normal saline $100{\mu}L$. Positive comparison group was injected with MIA and orally administered with indomethacin 5 mg/kg. Curcumae Longae Rhizoma pharmacopuncture low concentration (CL) group was induced for osteoarthritis by MIA and injected with Curcumae Longae Rhizoma pharmacopuncture low concentration $100{\mu}L$. Curcumae Longae Rhizoma pharmacopuncture high concentration (CH) group was induced for osteoarthritis by MIA and injected with Curcumae Longae Rhizoma pharmacopuncture high concentration $100{\mu}L$. Curcumae Longae Rhizoma pharmacopuncture was injected at ST35 and EX-LE4 each group (CL, CH). After that, hind paw weight distribution was measured and oxidative stress biomarker in serum, liver function biomarker in serum, western blot analysis were measured. Histological analysis of knee joint tissue was performed by hematoxylin and eosin staining, Safranin-O staining and Masson's trichrome staining. Results Hind paw weight distribution was significantly improved in both group. alanine aminotransferanse and aspartate aminotransferase were decreased significantly in CH group compare with Indomethacin threated group. Antioxidant enzyme glutathione peroxidase, Catalase and heme oxygenase-1 were increased in CH group compare with control group. Inflammatory cytokine cyclooxygenase-2, inducible nitric oxide synthase and interleukin-1 beta were decreased significantly in CH group. Histological analysis result shows that protective effects of joint and cartilage were observed in both CH and CL groups in a concentration-dependent. Conclusions The result suggest that Curcumae Longae Rhizoma pharmacopuncture has anti-oxidation effect, anti-inflammatory effect and also can prevent progression of osteoarthritis and protect joint cartilage.

• Journal of Ginseng Research
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• v.47 no.3
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• pp.376-384
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• 2023

Background: Hepatic lipid disorder impaired mitochondrial homeostasis and intracellular redox balance, triggering development of non-alcohol fatty liver disease (NAFLD), while effective therapeutic approach remains inadequate. Ginsenosides Rc has been reported to maintain glucose balance in adipose tissue, while its role in regulating lipid metabolism remain vacant. Thus, we investigated the function and mechanism of ginsenosides Rc in defending high fat diet (HFD)-induced NAFLD. Methods: Mice primary hepatocytes (MPHs) challenged with oleic acid & palmitic acid were used to test the effects of ginsenosides Rc on intracellular lipid metabolism. RNAseq and molecular docking study were performed to explore potential targets of ginsenosides Rc in defending lipid deposition. Wild type and liver specific sirtuin 6 (SIRT6, 50721) deficient mice on HFD for 12 weeks were subjected to different dose of ginsenosides Rc to determine the function and detailed mechanism in vivo. Results: We identified ginsenosides Rc as a novel SIRT6 activator via increasing its expression and deacetylase activity. Ginsenosides Rc defends OA&PA-induced lipid deposition in MPHs and protects mice against HFD-induced metabolic disorder in dosage dependent manner. Ginsenosides Rc (20mg/kg) injection improved glucose intolerance, insulin resistance, oxidative stress and inflammation response in HFD mice. Ginsenosides Rc treatment accelerates peroxisome proliferator activated receptor alpha (PPAR-α, 19013)-mediated fatty acid oxidation in vivo and in vitro. Hepatic specific SIRT6 deletion abolished ginsenoside Rc-derived protective effects against HFD-induced NAFLD. Conclusion: Ginsenosides Rc protects mice against HFD-induced hepatosteatosis by improving PPAR-α-mediated fatty acid oxidation and antioxidant capacity in a SIRT6 dependent manner, and providing a promising strategy for NAFLD.

• Korean Journal of Exercise Nutrition
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• v.16 no.2
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• pp.65-71
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• 2012

Oxygen is the final acceptor of electron transport from fat and carbohydrate oxidation, which is the rate-limiting factor for cellular ATP production. Under altitude hypoxia condition, energy reliance on anaerobic glycolysis increases to compensate for the shortfall caused by reduced fatty acid oxidation [1]. Therefore, training at altitude is expected to strongly influence the human metabolic system, and has the potential to be designed as a non-pharmacological or recreational intervention regimen for correcting diabetes or related metabolic problems. However, most people cannot accommodate high altitude exposure above 4500 M due to acute mountain sickness (AMS) and insulin resistance corresponding to a increased levels of the stress hormones cortisol and catecholamine [2]. Thus, less stringent conditions were evaluated to determine whether glucose tolerance and insulin sensitivity could be improved by moderate altitude exposure (below 4000 M). In 2003, we and another group in Austria reported that short-term moderate altitude exposure plus endurance-related physical activity significantly improves glucose tolerance (not fasting glucose) in humans [3,4], which is associated with the improvement in the whole-body insulin sensitivity [5]. With daily hiking at an altitude of approximately 4000 M, glucose tolerance can still be improved but fasting glucose was slightly elevated. Individuals vary widely in their response to altitude challenge. In particular, the improvement in glucose tolerance and insulin sensitivity by prolonged altitude hiking activity is not apparent in those individuals with low baseline DHEA-S concentration [6]. In addition, hematopoietic adaptation against altitude hypoxia can also be impaired in individuals with low DHEA-S. In short-lived mammals like rodents, the DHEA-S level is barely detectable since their adrenal cortex does not appear to produce this steroid [7]. In this model, exercise training recovery under prolonged hypoxia exposure (14-15% oxygen, 8 h per day for 6 weeks) can still improve insulin sensitivity, secondary to an effective suppression of adiposity [8]. Genetically obese rats exhibit hyperinsulinemia (sign of insulin resistance) with up-regulated baseline levels of AMP-activated protein kinase and AS160 phosphorylation in skeletal muscle compared to lean rats. After prolonged hypoxia training, this abnormality can be reversed concomitant with an approximately 50% increase in GLUT4 protein expression. Additionally, prolonged moderate hypoxia training results in decreased diffusion distance of muscle fiber (reduced cross-sectional area) without affecting muscle weight. In humans, moderate hypoxia increases postprandial blood distribution towards skeletal muscle during a training recovery. This physiological response plays a role in the redistribution of fuel storage among important energy storage sites and may explain its potent effect on changing body composition. Conclusion: Prolonged moderate altitude hypoxia (rangingfrom 1700 to 2400 M), but not acute high attitude hypoxia (above 4000 M), can effectively improve insulin sensitivity and glucose tolerance for humans and antagonizes the obese phenotype in animals with a genetic defect. In humans, the magnitude of the improvementvaries widely and correlates with baseline plasma DHEA-S levels. Compared to training at sea-level, training at altitude effectively decreases fat mass in parallel with increased muscle mass. This change may be associated with increased perfusion of insulin and fuel towards skeletal muscle that favors muscle competing postprandial fuel in circulation against adipose tissues.

• Food Science and Biotechnology
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• v.15 no.5
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• pp.728-734
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• 2006

The tannins represent a highly heterogeneous group of water-soluble plant polyphenols that may play an important role in antimutagenic and antioxidant properties. We investigated the antioxidant function of tannic acid in comparison to other phenolic compounds including catechin, chlorogenic acid, cinnamic acid, ellagic acid, and gallic acid for their ability to scavenge several stable radicals and reactive oxygen species (ROS) such as ${\bullet}DPPH^+$, ${\bullet}ABTS^+$, hydrogen peroxide, hydroxyl radical, and superoxide radical. The ability of tannic acid to decrease paraquat-induced lipid oxidation in mouse liver and lung through its antioxidant properties was also assessed. The results showed that almost all the tested compounds have stable radical scavenging activity except cinnamic acid. Tannic acid, gallic acid, and ellagic acid demonstrated remarkable ROS scavenging properties toward $H_2O_2$, ${\bullet}OH^-$, ${\bullet}O_2^-$ and especially only tannic acid could inhibit paraquat-induced lipid peroxidation effectively in mouse liver and lung. Based on these results, it appears that increased number of galloyl and ortho-hydroxyl groups enhances the antioxidant activity of phenolic compounds and tannic acid is evaluated as the most effective antioxidant among all the tested compounds. These results suggest that the tannins, especially tannic acid, can be used as therapeutic agent for various diseases caused by ROS.

• Molecules and Cells
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• v.37 no.10
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• pp.719-726
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• 2014

The ${\gamma}$-Aminobutyric acid (GABA) that is found in prokaryotic and eukaryotic organisms has been used in various ways as a signaling molecule or a significant component generating metabolic energy under conditions of nutrient limitation or stress, through GABA catabolism. Succinic semialdehyde dehydrogenase (SSADH) catalyzes the oxidation of succinic semialdehyde to succinic acid in the final step of GABA catabolism. Here, we report the catalytic properties and two crystal structures of SSADH from Streptococcus pyogenes (SpSSADH) regarding its cofactor preference. Kinetic analysis showed that SpSSADH prefers $NADP^+$ over $NAD^+$ as a hydride acceptor. Moreover, the structures of SpSSADH were determined in an apo-form and in a binary complex with $NADP^+$ at $1.6{\AA}$ and $2.1{\AA}$ resolutions, respectively. Both structures of SpSSADH showed dimeric conformation, containing a single cysteine residue in the catalytic loop of each subunit. Further structural analysis and sequence comparison of SpSSADH with other SSADHs revealed that Ser158 and Tyr188 in SpSSADH participate in the stabilization of the 2'-phosphate group of adenine-side ribose in $NADP^+$. Our results provide structural insights into the cofactor preference of SpSSADH as the gram-positive bacterial SSADH.

• Structural Engineering and Mechanics
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• v.16 no.6
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• pp.749-769
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• 2003

The structural deterioration of concrete structures due to reinforcement corrosion is a major worldwide problem. Service life of the age-degraded concrete structures is governed by the protective action provided by the cover concrete against the susceptibility of the reinforcement to the corrosive environment. The corrosion of steel would result in the various corrosion products, which depending on the level of the oxidation may have much greater volume than the original iron that gets consumed by the process of corrosion. This volume expansion would be responsible for exerting the expansive radial pressure at the steel-concrete interface resulting in the development of hoop tensile stresses in the surrounding cover concrete. Once the maximum hoop tensile stress exceeds the tensile strength of the concrete, cracking of cover concrete would take place. The cracking begins at the steel-concrete interface and propagates outwards and eventually resulting in the through cracking of the cover concrete. The cover cracking would indicate the loss of the service life for the corrosion-affected structures. In the present paper, analytical models have been developed considering the residual strength of the cracked concrete and the stiffness provided by the combination of the reinforcement and expansive corrosion products. The problem is modeled as a boundary value problem and the governing equations are expressed in terms of the radial displacement. The analytical solutions are presented considering a simple 2-zone model for the cover concrete viz. cracked or uncracked. A sensitivity analysis has also been carried out to show the influence of the various parameters of the proposed models. The time to cover cracking is found to be function of initial material properties of the cover concrete and reinforcement plus corrosion products combine, type of rust products, rate of corrosion and the residual strength of the cover concrete. The calculated cracking times are correlated against the published experimental and analytical reference data.