• Korean Chemical Engineering Research
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• v.44 no.4
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• pp.410-416
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• 2006

For highly efficient operation of a Bunsen process section in an iodine-sulfur thermochemical hydrogen production cycle using nuclear heat, the process characteristics of $H_2SO_4-HI-H_2-O-I_2$ mixture system for separating into two liquid phases ($H_2SO_4$-rich phase and $HI_x$-rich phase) and the distribution of $H_2O$ to each phase were investigated.The experiments for process variables were carried out in the temperature range, from 298 to 353 K, and in the $H_2SO_4/HI/H_2O/I_2$ molar ratio of 1/2/14~20/0.5~8.0. As the results, for the $SO_2-I_2-H_2O$ Bunsen reaction system, the ranges between the starting point and the saturation point for two liquid phases separation were determined by calculation. The best result for the minimization of impurities (HI and $I_2$ in $H_2SO_4$ phase and $H_2SO_4$ in $HI_x$ phase) in each phase was obtained in an optimum condition with the highest temperature of 353 K and the highest $I_2$ molar composition. In this condition, the $HI/H_2SO_4$ molar ratio in the $H_2SO_4$-rich phase and the $H_2SO_4/HI_x$ molar ratio in the $HI_x$-rich phase were 0.024 and 0.028, respectively. For the distribution of $H_2O$ to each phase, it is appeared that the affinity between $HI_x$ and $H_2O$ was more superior to that between $H_2SO_4$ and $H_2O$. The affinity between $HI_x$ and $H_2O$ was decreased with increasing temperature but increased with increasing $I_2$ molar composition.

• Journal of Life Science
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• v.29 no.9
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• pp.977-985
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• 2019

Aster yomena (Kitam.) Honda is an edible vegetable and perennial herb belonging to the Asteraceae family, and has been used for a long time for the prevention and treatment of various diseases. Although leaf extracts of A. yomena are known to have antioxidant and anti-inflammatory effects, accurate efficacy assessments are still inadequate. In this study, we investigated whether the antioxidant efficacy of ethanol extract of A. yomena leaf (EEAY) is correlated with the anti-inflammatory effect in RAW 264.7 macrophages. The results showed that EEAY significantly inhibited the hydrogen peroxide ($H_2O_2$)-induced growth inhibition in RAW 264.7 cells, which was associated with increased expression of nuclear factor erythroid 2-related factor-2 (Nrf2) and heme oxygenase-1 (HO-1). EEAY pretreatment also effectively prevented $H_2O_2$-induced reactive oxygen species generation and apoptosis through inhibition of caspase-3 activation and poly (ADP-ribose) polymerase degradation. Additionally, EEAY significantly increased the expression and production of interleukin-10, a representative anti-inflammatory cytokine, which was associated with increased expression of toll-like receptor 4 and myeloid differentiation factor 88 at transcriptional and translational levels. Furthermore, the increased production of nitric oxide (NO) by lipopolysaccharide was markedly abolished under the condition of EEAY pretreatment, and the inhibitory effect of NO production by EEAY was further increased by hemin, an HO-1 inducer. Overall, our results suggest that EEAY is able to activate the Nrf2/HO-1 signaling pathway to protect RAW 264.7 macrophages from oxidative and inflammatory stress.

• Biomolecules & Therapeutics
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• v.32 no.3
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• pp.329-340
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• 2024

Mangiferin is a kind of natural xanthone glycosides and is known to have various pharmacological activities. However, since the beneficial efficacy of this compound has not been reported in retinal pigment epithelial (RPE) cells, this study aimed to evaluate whether mangiferin could protect human RPE ARPE-19 cells from oxidative injury mimicked by hydrogen peroxide (H₂O₂). The results showed that mangiferin attenuated H₂O₂-induced cell viability reduction and DNA damage, while inhibiting reactive oxygen species (ROS) production and preserving diminished glutathione (GSH). Mangiferin also antagonized H₂O₂-induced inhibition of the expression and activity of antioxidant enzymes such as manganese superoxide dismutase and GSH peroxidase, which was associated with inhibition of mitochondrial ROS production. In addition, mangiferin protected ARPE-19 cells from H₂O₂-induced apoptosis by increasing the Bcl-2/Bax ratio, decreasing caspase-3 activation, and blocking poly(ADP-ribose) polymerase cleavage. Moreover, mangiferin suppressed the release of cytochrome c into the cytosol, which was achieved by interfering with mitochondrial membrane disruption. Furthermore, mangiferin increased the expression and activity of heme oxygenase-1 (HO-1) and nuclear factor-erythroid-2 related factor 2 (Nrf2). However, the inhibition of ROS production, cytoprotective and anti-apoptotic effects of mangiferin were significantly attenuated by the HO-1 inhibitor, indicating that mangiferin promoted Nrf2-mediated HO-1 activity to prevent ARPE-19 cells from oxidative injury. The results of this study suggest that mangiferin, as an Nrf2 activator, has potent ROS scavenging activity and may have the potential to protect oxidative stress-mediated ocular diseases.

• Biomolecules & Therapeutics
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• v.24 no.6
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• pp.581-588
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• 2016

Lonchocarpine is a phenylpropanoid compound isolated from Abrus precatorius that has anti-bacterial, anti-inflammatory, antiproliferative, and antiepileptic activities. In the present study, we investigated the antioxidant effects of lonchocarpine in brain glial cells and analyzed its molecular mechanisms. We found that lonchocarpine suppressed reactive oxygen species (ROS) production and cell death in hydrogen peroxide-treated primary astrocytes. In addition, lonchocarpine increased the expression of anti-oxidant enzymes, such as heme oxygenase-1 (HO-1), NAD(P)H:quinone oxidoreductase 1 (NQO1), and manganese superoxide dismutase (MnSOD), which are all under the control of Nrf2/antioxidant response element (ARE) signaling. Further, mechanistic studies showed that lonchocarpine increases the nuclear translocation and DNA binding of Nrf2 to ARE as well as ARE-mediated transcriptional activities. Moreover, lonchocarpine increased the phosphorylation of AMP-activated protein kinase (AMPK) and three types of mitogen-activated protein kinases (MAPKs). By treating astrocytes with each signaling pathway-specific inhibitor, AMPK, c-jun N-terminal protein kinase (JNK), and p38 MAPK were identified to be involved in lonchocarpine-induced HO-1 expression and ARE-mediated transcriptional activities. Therefore, lonchocarpine may be a potential therapeutic agent for neurode-generative diseases that are associated with oxidative stress.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.4
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• pp.479-491
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• 1998

In order to know the pathogenesis of adult respiratory distress syndrome (ARDS) in association with the oxidative stress by neutrophils, the role of platelet activating factor (1-0-alkyl-2-acetyl-snglycero-3-phosphocholine, PAF) was investigated during acute lung injury induced by interleukin- $1{\alpha}$ (IL-1) in rats. An insufflation of IL-1 into the rat's trachea increased the acetyltransferase activity in the lung and the increase of PAF content was followed. As evidences of acute lung injury by neutrophilic respiratory burst, lung leak index, myeloperoxidase activity, numbers of neutrophils in the bronchoalveolar lavage fluid, neutrophilic adhesions to endothelial cells and NBT positive neutrophils were increased after IL-1 treatment. In addition, a direct instillation of PAF into the trachea caused acute lung leak and the experimental results showed a similar pattern in comparison with IL-1 induced acute lung injury. For the confirmation of oxidative stress during acute lung leak by IL-1 and PAF, a histochemical electron microscopy was performed. In IL-1 and PAF treated lungs of rats, the deposits of cerrous perhydroxide were found. To elucidate the role of PAF, an intravenous injection of PAF receptor antagonist, WEB 2086 was given immediately after IL-1 or PAF treatment. WEB 2086 decreased the production of hydrogen peroxide and the acute lung leak. In ultrastructural study, WEB 2086 mitigated the pathological changes induced by IL-1 or PAF. The nuclear factor kappa B (NFkB) was activated by PAF and this activation was inhibited by WEB 2086 almost completely. Based on these experimental results, it is suggested that the PAF produced in response to IL-1 through the remodeling pathway has the major role for acute lung injury by neutrophilic respiratory burst. In an additional experiment, we can also come to conclude that the activation of the NFkB by PAF is thought to be the fundamental mechanism to initiate the oxidative stress by neutrophils causing release of proinflammatory cytokines and activation of phospholipase $A_2$.

• Korean Journal of Air-Conditioning and Refrigeration Engineering
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• v.20 no.4
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• pp.266-273
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• 2008

Natural gas hydrates are ice-like solid substances, which are composed of water and natural gas, mainly methane. They have three kinds of crystal structures of five polyhedra formed by hydrogen-bonded water molecules, and are stable at high pressures and low temperatures. They contain large amounts of organic carbon and widely occur in deep oceans and permafrost regions. Therefore, they are expected as a potential energy resource in the future. Especially, $1m^3$ natural gas hydrate contains up to $172Nm^3$ of methane gas, de pending on the pressure and temperature of production. Such large volumes make natural gas hydrates can be used to store and transport natural gas. In this study, three-phase equilibrium conditions for forming natural gas hydrate were numerically obtained in pure water and single electrolyte solution containing 3 wt% NaCl. The results show that the predictions match the previous experimental values very well, and it was found that NaCl acts as an inhibitor. Also, help gases such that ethane, propane, i-butane, and n-butane reduce the hydrate formation pressure at the same temperature.

• Journal of Ginseng Research
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• v.47 no.2
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• pp.311-318
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• 2023

Background: The beneficial effects of compound K (CK) on different chronic diseases have been shown to be at least related to antioxidant action. Nevertheless, since its antioxidant activity in human retinal pigment epithelial (RPE) cells is still unknown, here we investigated whether CK alleviates oxidative stress-stimulated damage in RPE ARPE-19 cells. Methods: The cytoprotective consequence of CK in hydrogen peroxide (H₂O₂)-treated cells was evaluated by cell viability, DNA damage, and apoptosis assays. Fluorescence analysis and immunoblotting were performed to investigate the inhibitory action of CK on reactive oxygen species (ROS) production and mitochondrial dysfunction. Results: H₂O₂-promoted cytotoxicity, oxidative stress, DNA damage, mitochondrial impairment, and apoptosis were significantly attenuated by CK in ARPE-19 cells. Furthermore, nuclear factor erythroid 2-related factor 2 (Nrf2) phosphorylation level and its shuttling to the nucleus were increased, which was correlated with upregulated activation of heme oxygenase-1 (HO-1). However, zinc protoporphyrin, a blocker of HO-1, significantly abrogated the preventive action of CK in H₂O₂-treated ARPE-19 cells. Conclusion: This study indicates that activation of Nrf2/HO-1 signaling by CK plays an important role in rescuing ARPE-19 cells from oxidative cellular damage.

• Asian-Australasian Journal of Animal Sciences
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• v.29 no.2
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• pp.288-298
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• 2016

Resveratrol acts as a free radical scavenger and a potent antioxidant in the inhibition of numerous reactive oxygen species (ROS). The function of resveratrol and resveratrol-loaded nanoparticles in protecting human lung cancer cells (A549) against hydrogen peroxide was investigated in this study. The 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid (ABTS) assay was performed to evaluate the antioxidant properties. Resveratrol had substantially high antioxidant capacity (trolox equivalent antioxidant capacity value) compared to trolox and vitamin E since the concentration of resveratrol was more than $50{\mu}M$. Nanoparticles prepared from ${\beta}$-lactoglobulin (${\beta}$-lg) were successfully developed. The ${\beta}$-lg nanoparticle showed 60 to 146 nm diameter in size with negatively charged surface. Non-cytotoxicity was observed in Caco-2 cells treated with ${\beta}$-lg nanoparticles. Fluorescein isothiocynate-conjugated ${\beta}$-lg nanoparticles were identified into the cell membrane of Caco-2 cells, indicating that nanoparticles can be used as a delivery system. Hydrogen peroxide caused accumulation of ROS in a dose- and time-dependent manner. Resveratrol-loaded nanoparticles restored $H_2O_2$-induced ROS levels by induction of cellular uptake of resveratrol in A549 cells. Furthermore, resveratrol activated nuclear factor erythroid 2-related factor 2-Kelch ECH associating protein 1 (Nrf2-Keap1) signaling in A549 cells, thereby accumulation of Nrf2 abundance, as demonstrated by western blotting approach. Overall, these results may have implications for improvement of oxidative stress in treatment with nanoparticles as a biodegradable and non-toxic delivery carrier of bioactive compounds.

• Applied Chemistry for Engineering
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• v.8 no.3
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• pp.430-437
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• 1997

Uranyl-peroxide compound was prepared by the reaction of excess hydrogen peroxide solution and trace uranium in filtrate from nuclear fuel conversion plant. The $CO_3{^{2-}}$ in filtrate was removed first by heating more than $98^{\circ}C$, because uranyl-peroxide compound could not be precipitated by $CO_3{^{2-}}$ remaining in filtrate. The optimum condition for uranyl-peroxide compound was ageing for 1 hr after controling the pH with $NH_3$ gas and adding the excess $H_2O_2$ of 10ml/lit.-filtrate. Uranium concentration in the filtrate was appeared to 3 ppm after the precipitation of uranyl-peroxide compound, and the chemical composition of this compound was analyzed to $UO_4{\cdot}2NH_4F$ with FT-IR, X-ray diffractometry, TG and chemical analysis. Also, this fine particle, about $1{\sim}2{\mu}m$, could be grown up to $4{\mu}m$ at pH 9.5 and $60^{\circ}C$. The separation efficiency of precipitate from mother liquor was increased with increase of pH and reaction temperature. Otherwise, the crystal form of this particle showed octahedral by SEM and XRD, and $U_3O_8$ powder was obtained by thermal decomposition at $650^{\circ}C$ in air atmosphere.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2019.10a
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• pp.92-92
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• 2019

Excessive or chronic inflammation contributes to the pathogenesis of many inflammatory diseases such as sepsis, rheumatoid arthritis, and ulcerative colitis. Hibiscus syriacus L. has been used as a medicinal plant in many Asian countries, even though its anti-inflammatory activity has been unclear. Therefore, we investigated the anti-inflammatory effect of anthocyanin fractions from the H. syriacus L. varieties Pulsae (PS) on the lipopolysaccharide (LPS)-induced expression of proinflammatory mediators and cytokines in RAW264.7 macrophages. PS suppressed LPS-induced nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$) secretion concomitant with downregulation of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) expression. Furthermore, PS inhibited the production of proinflammatory cytokines such as tumor necrosis factor-alpha ($TNF-{\alpha}$), interleukin-6 (IL-6), and IL-12 in LPS-stimulated RAW264.7 macrophages. Further study showed that PS significantly decreased LPS-induced nuclear translocation of the nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$) subunits, p65 and p50. Molecular docking data showed that many anthocyanins from PS fit into the hydrophobic pocket of MD2 and bound to Toll-like receptor 4 (TLR4), indicating that PS inhibits the TLR4-MD2-mediated inflammatory signaling pathway. Especially, apigenin-7-O-glucoside most powerfully bound to MD2 and TLR4 through LYS122, LYS122, and SER127 at a distance of $2.205{\AA}$, $3.098{\AA}$, and $2.844{\AA}$ and SER441 at a distance of $2.873{\AA}$ (docking score: -8.4) through hydrogen bonding, respectively. Additionally, PS inhibited LPS-induced TLR4 dimerization/expression on the cell surface, which consequently decreased MyD88 recruitment and IRAK4 phosphorylation. PS completely blocked LPS-mediated mortality in zebrafish larvae by diminishing the recruitment of neutrophil and macrophages accompanied by low levels of proinflammatory cytokines. Taken together, our results indicate that PS attenuates LPS-mediated inflammation in both in vitro and in vivo by blocking the TLR4/MD2-MyD88/IRAK4-$NF-{\kappa}B$ axis. Therefore, PS might be used as a novel modulatory candidate for effective treatment of LPS-mediated inflammatory diseases.