• Nutrition Research and Practice
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• v.1 no.2
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• pp.105-112
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• 2007

Ascorbic acid has been reported to extend replicative life span of human embryonic fibroblast (HEF). Since the detailed molecular mechanism of this phenomenon has not been investigated, we attempted to elucidate. Continuous treatment of HEF cells with ascorbic acid at ($200{\mu}M$) from 40 population doubling (PD) increased maximum PD numbers by 18% and lowered $SA-{\beta}-gal$ positive staining, an aging marker, by 2.3 folds, indicating that ascorbic acid extends replicative life span of HEF cells. Ascorbic acid treatment lowered DCFH by about 7 folds and Rho123 by about 70%, suggesting that ascorbic acid dramatically decreased ROS formation. Ascorbic acid also increased aconitase activity, a marker of mitochondrial aging, by 41%, indicating that ascorbic acid treatment restores age-related decline of mitochondrial function. Cell cycle analysis by flow cytometry revealed that ascorbic acid treatment decreased G1 population up to 12%. Further western blot analysis showed that ascorbic acid treatment decreased levels of p53, phospho-p53 at ser 15, and p21, indicating that ascorbic acid relieved senescence-related G1 arrest. Analysis of AP (apurinic/apyrimidinic) sites showed that ascorbic acid treatment decreased AP site formation by 35%. We also tested the effect of hydrogen peroxide treatment, as an additional oxidative stress. Continuous treatment of $20{\mu}M$ of hydrogen peroxide from PD 40 of HEF cells resulted in premature senescence due to increased ROS level, and increased AP sites. Taken together, the results suggest that ascorbic acid extends replicative life span of HEF cells by reducing mitochondrial and DNA damages through lowering cellular ROS.

• Microbiology and Biotechnology Letters
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• v.45 no.3
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• pp.236-242
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• 2017

The conversion of marine biomass to renewable energy has been considered an alternative to fossil fuels. Butanol, in particular, can be used directly as a fuel. In this experiment, the brown alga Undaria pinnatifida was selected as a biomass for biobutanol production. Hyper thermal (HT) acid hydrolysis was used as an acid hydrolysis method to produce monosaccharides. The optimal pretreatment conditions for U. pinnatifida were determined as slurry with 10% (w/v) U. pinnatifida content and 270 mM $H_2SO_4$, and heating at $160^{\circ}C$ for 7.5 min. Enzymatic saccharification was carried out with Celluclast 1.5 L, Viscozyme L, and Ultraflo Max. The optimal saccharification condition was 12 U/ml Viscozyme L. Fermentations were carried out for the production of acetone, butanol, and ethanol by Clostridium acetobutylicum KCTC 1724, Clostridium beijerinckii KCTC 1785, and Clostridium tyrobutyricum KCTC 5387. The fermentations were carried out using a pH-control. The optimal ABE fermentation condition determined using C. acetobutylicum KCTC 1724 adapted to 160 g/l mannitol. An ABE concentration of 9.05 g/l (0.99 g/l acetone, 5.62 g/l butanol, 2.44 g/l ethanol) was obtained by the consumption of 24.14 g/l monosaccharide with $Y_{ABE}$ of 0.37 in pH 5.0.

• Journal of Nutrition and Health
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• v.42 no.8
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• pp.673-681
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• 2009

Diabetes mellitus is a multifactorial disease. Particularly, diabetic nephropathy is a serious complication for diabetic patients, yet the precise mechanisms that underline the initial stage of diabetic renal inflammation remain unknown. However, oxidative stress induced by hyperglycemia in diabetes is implicated in diabetic renal disease. We hypothesized that dietary supplementation of antioxidants either VCE (0.5% VC + 0.5% VE) or Comb (0.5% VC + 0.5% VE + 2.5% N-acetylcysteine) improves acute diabetic renal inflammation through modulation of blood glucose levels and antioxidant and anti-inflammatory responses. Experimental animals (5.5 weeks old female ICR) used were treated with alloxan (180 mg/kg) once. When fasting blood glucose levels were higher than 250 mg/dL, mice were divided into 3 groups fed different levels of antioxidant supplementation, DM (diabetic mice fed AIN 93G purified rodent diet); VCE (diabetic mice fed 0.5% vitamin C and 0.5% vitamin E supplemented diet); Comb (diabetic mice fed 0.5% vitamin C, 0.5% vitamin E and 2.5% N-acetylcysteine supplemented diet), for 10 days and then sacrificed. Body weights were measured once a week and blood glucose levels were monitored twice a week. Lipid peroxidation products, thiobarbituric acid reacting substances were measured in kidney. NF-${\kappa}B$ activation was indirectly demonstrated by pI${\kappa}B$-${\alpna}$ and expressions of selective inflammatory and oxidative stress markers including antioxidant enzymes were also determined. Dietary antioxidant supplementation improved levels of blood glucose as well as kidney lipid peroxi-dation. Dietary antioxidant supplementation improved NF-${\kappa}B$ activation and protein expression of HO-1, but not mRNA expression levels in diabetic mice fed Comb diet. In contrast, the mRNA and protein expression of CuZnSOD was decreased in diabetic mice fed Comb diet. However, antioxidant supplementation did not improve mRNA and protein expressions of IL-$1{\beta}$ and MnSOD in diabetic mice. These findings demonstrate that acute diabetic renal inflammation was associated with altered inflammatory and antioxidant responses and suggest that antioxidant cocktail supplementation may have beneficial effects on early stage of diabetic nephropathy through modulation of blood glucose levels and antioxidant enzyme expressions.

• Archives of Pharmacal Research
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• v.28 no.6
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• pp.709-715
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• 2005

The purpose of this study was to investigate the effect of atropine on peripheral vasodilation and the mechanisms involved. The isometric tension of rat mesenteric artery rings was recorded in vitro on a myograph. The results showed that atropine, at concentrations greater than 1$\mu$M, relaxed the noradrenalin (NA)-precontracted rat mesenteric artery in a concentration-dependent manner. Atropine-induced vasodilatation was mediated, in part, by an endothelium-dependent mechanism, to which endothelium-derived hyperpolarizing factor may contribute. Atropine was able to shift the NA-induced concentration-response curve to the right, in a non-parallel manner, suggesting the mechanism of atropine was not mediated via the ${\alpha}_1$-adrenoreceptor. The $\beta$-adrenoreceptor and ATP sensitive potassium channel, a voltage dependent calcium channel, were not involved in the vasodilatation. However, atropine inhibited the contraction derived from NA and $CaCl_2$ in $Ca^{2+}$-free medium, in a concentration dependent manner, indicating the vasodilatation was related to the inhibition of extracellular $Ca^{2+}$ influx through the receptor-operated calcium channels and intracellular $Ca^{2+}$ release from the $Ca^{2+}$ store. Atropine had no effect on the caffeine-induced contraction in the artery segments, indicating the inhibition of intracellular $Ca^{2+}$ release as a result of atropine most likely occurs via the IP3 pathway rather than the ryanodine receptors. Our results suggest that atropine-induced vasodilatation is mainly from artery smooth muscle cells due to inhibition of the receptor-mediated $Ca^{2+}$-influx and $Ca^{2+}$-release, and partly from the endothelium mediated by EDHF.

• YAKHAK HOEJI
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• v.53 no.5
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• pp.286-292
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• 2009

In this study, we investigated the anti-obese activity of HPJ extract in C57BL/6J mice. The C57BL/6J mice were randomly divided into five groups: normal control group (Con), high fat diet control group (HFD), treatment groups with HPJ at 125 mg/kg (HPJ125), 250 mg/kg (HPJ250), or 500 mg/kg (HPJ500). To induce an obesity, mice were fed by a high fat diet for 6 weeks, and mice were administered with HPJ extract once a day for 8 weeks. At the end of treatment, we examined the effect of HPJ extract on body weight, plasma lipid, and lipogenic enzymes. HPJ extract was found to lower whole body and epididymal adipose tissue weights and lowered plasma levels of glucose, insulin, triglyceride (TG), total cholesterol (TC), non-esterified fatty acid (NEFA) and leptin, compared to those in HFD group. Histological analyses of the liver and fat tissues of mice treated with HPJ extract revealed significantly decreased number of lipid droplets and decreased size of adipocytes compared to the HFD group. In addition, HPJ extract preserved the morphological integrity of pancreatic islets. To elucidate an action mechanism of HPJ extract, Western blot and RT-PCR were performed using epididymal adipose tissues. HPJ extract up-regulated the levels of phosphorylated adenosine monophosphate-activated protein kinase (AMPK) and its substrate, acetyl-CoA carboxylasse (ACC). HPJ extract also attenuated lipogenic gene expressions of sterol regulatory element-binding protein $1{\alpha}$ (SREBP$1{\alpha}$), fatty acid synthase (FAS), sterol-CoA desaturase 1 (SCD1) and glycerol-3-phosphate acyltransferase (GPAT) in dose-dependent manners. In contrast, expressions of lipolytic genes such as peroxisome proliferator-activated receptor-$\alpha$ (PPAR-${\alpha}$) and CD36, and fatty acid $\beta$-oxidation gene, carnitine palmitoyltransferase-1 (CPT-1) were increased. These results suggest that HPJ extract ameliorates obesity through inhibiting synthesis of lipogenic enzymes as well as stimulating fatty acid oxidation resulting from activation of AMPK, and HPJ extract could be developed as a potential therapeutic agent for obese patients.

• Journal of Ginseng Research
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• v.44 no.6
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• pp.790-798
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• 2020

Background: Beneficial effects of Korean Red Ginseng (KRG) on polycystic ovarian syndrome (PCOS) remains unclear. Methods: We examined whether pretreatment (daily from 2 hours before PCOS induction) with KRG extract in water (KRGE; 75 and 150 mg/kg/day, p.o.) could exert a favorable effect in a dehydroepian-drosterone (DHEA)-induced PCOS rat model. Results: Pretreatment with KRGE significantly inhibited the elevation of body and ovary weights, the increase in number and size of ovarian cysts, and the elevation of serum testosterone and estradiol levels induced by DHEA. Pretreatment with KRGE also inhibited macrophage infiltration and enhanced mRNA expression levels of chemokines [interleukin (IL)-8, monocyte chemoattractant protein-1), proinflammatory cytokines (IL-1β, IL-6), and inducible nitric oxide synthase in ovaries induced by DHEA. It also prevented the reduction in mRNA expression of growth factors (epidermal growth factor, transforming growth factor-beta (EGF, TGF-β)) related to inhibition of the nuclear factor kappa-light-chain-enhancer of activated B cell pathway and stimulation of the nuclear factor erythroid-derived 2-related factor 2 pathway. Interestingly, KRGE or representative ginsenosides (Rb1, Rg1, and Rg3(s)) inhibited the activity of inflammatory enzymes cyclooxygenase-2 and iNOS, cytosolic p-IκB, and nuclear p-nuclear factor kappa-light-chain-enhancer of activated B in lipopolysaccharide-induced RAW264.7 cells, whereas they increased nuclear factor erythroid-derived 2-related factor 2 nuclear translocation. Conclusion: These results provide that KRGE could prevent DHEA-induced PCOS via antiinflammatory and antioxidant activities. Thus, KRGE may be used in preventive and therapeutic strategies for PCOS-like symptoms.

• Proceedings of the Materials Research Society of Korea Conference
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• 2011.05a
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• pp.15-15
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• 2011

As you know, boron compounds, borax ($Na_2B_4O_5(OH)_4{\cdot}8H_2O$) etc. were known thousands of years ago. As for natural boron, it has two naturally occurring and stable isotopes, boron 11 ($^{11}B$) and boron 10 ($^{10}B$). The neutron absorption $^{10}B$ is included about 19~20% with 80~81% $^{11}B$. Boron is similar to carbon in its capability to form stable covalently bonded molecular networks. The mass difference results in a wide range of ${\beta}$ values between the $^{11}B$ and $^{10}B$. The $^{10}B$ isotope, stable with 5 neutrons is excellent at capturing thermal neutrons. For example, it is possible to decrease a thermal neutron required for the nuclear reaction of uranium 235 ($^{235}U$). If $^{10}B$ absorbs a neutron ($^1n$), it will change to $^7Li+^1{\alpha}$ (${\alpha}$ ray, like $^4He$) with prompt ${\gamma}$ ray from $^{11}B$ $^{11}B$ (equation 1). $$^{10}B+^1n\;{\rightarrow}\;^{11}B\;{\rightarrow}\; prompt \;{\gamma}\;ray (478 keV), \;^7Li+4{\alpha}\;(4He)\;\;\;\;{\cdots}\; (1)$$ If about 1% boron is added to stainless steel, it is known that a neutron shielding effect will be 3 times the boron free steel. Enriched boron or $^{10}B$ is used in both radiation shielding and in boron neutron capture therapy. Then, $^{10}B$ is used for reactivity control and in emergency shutdown systems in nuclear reactors. Furthermore, boron carbide, $B_4C$, is used as the charge of a nuclear fission reaction control rod material and neutron cover material for nuclear reactors. The $B_4C$ powder of natural B composition is used as a charge of a control material of a boiling water reactor (BWR) which occupies commercial power reactors in nuclear power generation. The $B_4C$ sintered body which adjusted $^{10}B$ concentration is used as a charge of a control material of the fast breeder reactor (FBR) currently developed aiming at establishment of a nuclear fuel cycle. In this study for new boron compound, silicon boride ceramics for capturing thermal neutrons, preparation and characterization of both silicon tetraboride ($SiB_4$) and silicon hexaboride ($SiB_6$) and ceramics produced by sintering were investigated in order to determine the suitability of this material for nuclear power generation. The relative density increased with increasing sintering temperature. With a sintering temperature of 1,923 K, a sintered body having a relative density of more than 99% was obtained. The Vickers hardness increased with increasing sintering temperature. The best result was a Vickers hardness of 28 GPa for the $SiB_6$ sintered at 1,923K for 1 h. The high temperature Vickers hardness of the $SiB_6$ sintered body changed from 28 to 12 GPa in the temperature range of room temperature to 1,273 K. The thermal conductivity of the SiB6 sintered body changed from 9.1 to 2.4 W/mK in the range of room temperature to 1,273 K.

• Korean Journal of Veterinary Research
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• v.48 no.3
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• pp.327-336
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• 2008

Many herbal extracts have been reported to have a preventive or therapeutic effect of on diabetes mellitus. Momordica Charantia commonly known as bitter melon or karela has been reported to be a medicinal plant for treating various diseases including cancers and diabetes. The objectives of this study were to investigate anti-diabetic effects of bitter melon (BM) as determined by blood glucose levels, glucose tolerance test (GTT), insulin tolerance test (ITT), insulin and HbA1C activities in serum, serum biochemical and lipid levels, histopathology, immunohistochemistry and AMPK-${\alpha}2$ expression of skeletal muscle in male C57BL/6J db/db mice. There were four experimental groups including vehicle control, BM 10 mg/kg, BM 50 mg/kg, and BM 250 mg/kg. BM at doses of 10, 50, and 250 mg/kg was orally administered to the diabetic mice everyday for 8 weeks. The treatments of BM 10, 50, and 250 mg/kg significantly decreased the blood glucose level in the diabetic mice compared with vehicle control (p < 0.05). The treatments of BM 10 and 50 mg/kg significantly decreased the GTT, ITT and HbA1c levels in the diabetic mice compared with vehicle control (p < 0.05). All BM groups significantly decreased GOT, GPT, BUN, LDL and glucose levels in the diabetic mice compared with the vehicle control mice (p < 0.05). The livers of mice treated with the BM 10, 50, and 250 mg/kg showed a remarkable decrease in the number of lipid droplets compared with the vehicle control. The pancreas of mice treated with the BM 10, 50, and 250 mg/kg showed a remarkable increase in insulin concentration of ${\beta}$-cells compared with the vehicle control. In addition, the treatments of BM 10, 50, and 250 mg/kg actually increased the expression of AMPK-${\alpha}2$ compared with vehicle control. These results suggest that BM has a respectable anti-diabetic effect resulting from inhibition of blood glucose level and lipid level in serum and that consumption of BM may give a benefit for controlling diabetes mellitus in humans.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.35 no.5
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• pp.294-298
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• 2009

Purpose: The development of a microvascularization is important for the homeostasis of normal bone. Vascular endothelial growth factor (VEGF) is one of the most important factors in vessel formation. The purpose of this study was to examine VEGF-related autocrine growth in periosteal-derived cells. Materials and methods: Periosteal-derived cells were obtained from mandibular periosteums and introduced into the cell culture. After passage 3, the periosteal-derived cells were further cultured for 21 days in an osteogenic inductive culture medium containing dexamethasone, ascorbic acid, and $\beta$-glycerophosphate. Results: The expression of four VEGF isoforms and VEGFRs was observed in periosteal-derived cells. Treatment with cultures with VEGFR-1 and VEGFR-2 Kinase Inhibitor inhibited osteoblastic differentiation and alkaline phosphatase (ALP) activity of periosteal-derived cells. In addition, exogenous VEGF treatment increased calcium content in the periosteal-derived cells. Conclusion: These results suggest that VEGF might act as an autocrine growth molecule during osteoblastic differentiation of cultured human periosteal-derived cells.

• Journal of Environmental Health Sciences
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• v.46 no.2
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• pp.136-149
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• 2020

Objectives: The purpose of this study was to perform an aggregate human risk assessment for benzene in an industrial complex using the CalTOX model and to improve the reliability and predictability of the model by analyzing the uncertainty and sensitivity of the predicted assessment results. Methods: The CalTOX^TM 4.0 beta model was used to evaluate a selected region, and @Risk 7.6 software was used to analyze uncertainty and sensitivity. Results: As a result of performing the aggregate risk assessment on the assumption that 6.45E+04 g/d of benzene would be emitted into the atmosphere over two decades, 3% of the daily source term to air remained in the selected region, and 97% (6.26E+04 g/d) moved out of the region. As for exposure by breathing, the predicted LADD_inhalation was 2.14E-04 mg/kg-d, and that was assessed as making a 99.99% contribution to the LADD_total. Regarding human Risk_cancer assessment, the predicted human cancer risk was 5.19E-06 (95% CI; 4.07E-06-6.81E-06) (in the 95th percentile corresponding to the highest exposure level, a confidence interval of 90%). As a result of analyzing sensitivity, 'source term to air' was identified as the most influential variable, followed by 'exposure time, active indoors (h/day)', and 'exposure duration (years)'. Conclusions: As for the results of the human cancer risk assessment for the selected region, the predicted human cancer risk was 5.19E-06 (95% CI; 4.07E-06-6.81E-06) (in the 95th percentile, corresponding to the highest exposure level, a confidence interval of 90%). As a result of analyzing sensitivity, 'source term to air' was found to be most influential.