• 한국수산과학회지
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• 제48권6호
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• pp.888-897
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• 2015

The anti-inflammatory effect of alginate oligosaccharides on LPS-induced RAW 264.7 cells was investigated at different time points (0-60 h). The alginate oligosaccharides were produced by an alginate-degrading enzyme from Shewanella oneidensis PKA1008. The alginate oligosaccharides decreased the production of nitric oxide and proinflammatory cytokines [tumor necrosis factor-${\alpha}$, interleukin (IL)-$1{\beta}$, and IL-6] in a dose-dependent manner. The alginate oligosaccharides showed peak anti-inflammatory activity after 36 h of incubation; at that time point, reduced protein expression of NF-${\kappa}B$ p65, iNOS, and COX-2 was detected. Furthermore, the alginate oligosaccharide treatment reduced the formation of ear edema at 36 h compared to samples examined at 0 h when the oligosaccharides were administered at 50 and 250 mg/kg body weight, as well as dermal thickness and mast cell numbers in a histological analysis. These results suggest that alginate oligosaccharides are a promising anti-inflammatory agent.

• International Journal of Oral Biology
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• 제39권4호
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• pp.207-213
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• 2014

Antimicrobial actions of reactive oxygen/nitrogen species (ROS/RNS) derived from products of NADPH oxidase and inducible nitric oxide (NO) synthase in host phagocytes inactivate various bacterial macromolecules. To cope with these cytotoxic radicals, pathogenic bacteria have evolved to conserve systems necessary for detoxifying ROS/RNS and repairing damages caused by their actions. In response to these stresses, bacteria also induce expression of molecular chaperones to aid in ameliorating protein misfolding. In this study, we explored the function of a newly identified chaperone Spy, that is localized exclusively in the periplasm when bacteria exposed to conditions causing spheroplast formation, in the resistance of Salmonella Typhimurium to ROS/RNS. A spy deletion mutant was constructed in S. Typhimurium by a PCR-mediated method of one-step gene inactivation with ${\lambda}$ Red recombinase, and subjected to ROS/RNS stresses. The spy mutant Salmonella showed a modest decrease in growth rate in NO-producing cultures, and no detectable difference of growth rate in $H_2O_2$ containing cultures, compared with that of wild type Salmonella. Quantitative RT-PCR analysis showed that spy mRNA levels were similar regardless of both stresses, but were increased considerably in Salmonella mutants lacking the flavohemoglobin Hmp, which are incapable of NO detoxification, and lacking an alternative sigma factor RpoS, conferring hypersusceptibility to $H_2O_2$. Results demonstrate that Spy expression can be induced under extreme conditions of both stresses, and suggest that the protein may have supportive roles in maintaining proteostasis in the periplasm where various chaperones may act in concert with Spy, thereby protecting bacteria against toxicities of ROS/RNS.

• Journal of Microbiology and Biotechnology
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• 제18권1호
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• pp.145-152
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• 2008

A cell-based in vitro exposure system was developed to determine whether oxidative stress plays a role in the cytotoxic effects of volatile organic compounds (VOCs) such as benzene, toluene, xylene, and chlorobenzene, using human epithelial HeLa cells. Thin films based on cysteine-terminated synthetic oligopeptides were fabricated for immobilization of the HeLa cells on a gold (Au) substrate. In addition, an immobilized cell-based sensor was applied to the electrochemical detection of the VOCs. Layer formation and immobilization of the cells were investigated with surface plasmon resonance (SPR), cyclic voltammetry (CV), and electrochemical impedance spectroscopy (EIS). The adhered living cells were exposed to VOCs; this caused a change in the SPR angle and the VOC-specific electrochemical signal. In addition, VOC toxicity was found to correlate with the degree of nitric oxide (NO) generation and EIS. The primary reason for the marked increase in impedance was the change of aqueous electrolyte composition as a result of cell responses. The p53 and NF-${\kappa}B $ downregulation were closely related to the magnitude of growth inhibition associated with increasing concentrations of each VOC. Therefore, the proposed cell immobilization method, using a self-assembly technique and VOC-specific electrochemical signals, can be applied to construct a cell microarray for onsite VOC monitoring.

• The Korean Journal of Physiology and Pharmacology
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• 제1권4호
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• pp.393-402
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• 1997

In the present study, we characterized the angiotensin II (AII)-induced relaxations in the phenylephrine-precontracted rabbit mesenteric arteries with endothelium. 1) AII-induced relaxation was consistently observed in the rabbit mesenteric arteries with and without endothelium, but not in the aortic segment with endothelium. 2) AII-induced endothelium-dependent relaxation was markedly inhibited by $N^w-nitro-L-arginine$ (L-NNA, $100\;{\mu}M$), methylene blue ($10\;{\mu}M$) and LY83583 ($10\;{\mu}M$), respectively. 3) Inhibition of cyclooxygenase with indomethacin ($10\;{\mu}M$) strongly decreased the vasorelaxant response to AII irrespective of the presence of endothelium. 4) 7-Ethoxyresorufin ($1\;{\mu}M$) and clotrimazole ($1\;{\mu}M$), inhibitors of cytochrome P-450-dependent arachidonic acid metabolism, greatly attenuated the vasodilator response to AII. 5) Carbacyclin, arachidonic acid and prostaglandin $F_{2{\alpha}}$ ($PGF_{2{\alpha}}$) caused concentration-dependent relaxations in the mesenteric artery with endothelium, which were inhibited by L-NNA and methylene blue. 6) AII and $PGF_{2{\alpha}}$ significantly stimulated cyclic GMP formation in the mesenteric arteries with endothelium, which was inhibited by L-NNA and methylene blue, respectively. 7) AII enhanced synthesis of $PGF_{2{\alpha}}$ and 6-keto $PGF_{1{\alpha}}$ from the arterial segments with endothelium, which was inhibitable by indomethacin, but not by L-NNA. In conclusion, the vasorelaxant responses to AII of the rabbit mesenteric artery with endothelium are subserved by arachidonic acid and its metabolites produced via activation of cyclooxygenase and cytochrome P-450 enzyme as well as by nitric oxide.

• 공업화학
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• 제1권2호
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• pp.207-214
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• 1990

자동차 배기가스 정화용 촉매계에서 중요하게 취급되는 CO와 NO와의 산화환원반응을 다결정 Pt 표면위에서 초고진공계를 이용한 열탈착분광법(TDS)과 정상상태 실험을 통하여 알아 보았다. CO와 NO의 압력이 각각 $1{\times}10^{-7}Torr$로 일정할 때 $CO_2$의 생성속도는 560K 에서 최대값을 보였으며, 반응온도가 560K, NO 압력이 $1{\times}10^{-7}Torr$로 일정할 때, $CO_2$ 생성속도는 CO의 압력에 대하여 $1.35{\times}10^{-7}Torr$를 전후하여 1차에서 -0.3차로 변화하였다. 하지만 이 반응에 미치는 반응물의 압력에 의한 영향은 표면흡착질의 농도에 따라 달리 해석되어야 함을 알 수 있었다. 본 실험의 결과를 종합하여 다결정 Pt 상에서의 CO와 NO와의 반응에 대한 새로운 반응기구를 제안하였다.

• Natural Product Sciences
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• 제23권1호
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• pp.61-68
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• 2017

This study was performed to investigate the ameliorating effects of steamed soybeans (SS) and fermented SS (FSS) on lipid metabolism in high-fat diet-induced obese mice. ICR mice were divided into four groups and given the following different diets: normal diet (ND), high-fat diet (HFD), HFD with 1% SS (HFD + SS), and HFD with 1% FSS (HFD + FSS). After 14 weeks, the body weight gain was higher in the HFD group compared with the ND group but lower in the HFD + FSS group compared with the HFD group. Plasma levels of triglyceride (TG), total cholesterol (TC), low density lipoprotein-cholesterol, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were significantly higher in the HFD group compared to the ND group, but lower in the HFD + SS and HFD + FSS groups compared with the HFD group. In addition, leptin concentration in plasma was lower in the groups fed HFD + SS and HFD + FSS compared with the HFD group. The accumulation of hepatic TG and TC was significantly inhibited in the HFD + SS and HFD + FSS groups. Furthermore, SS and FSS attenuated lipid peroxidation and nitric oxide formation in the liver induced by the high-fat diet. These results suggest that soybeans, especially FSS, may be useful in preventing obesity-induced abnormalities in lipid metabolism.

• 대한본초학회지
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• 제23권1호
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• pp.29-38
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• 2008

Objectives : Evodia officinalis DODE (EO), an herbal plant, has been widely used in traditional Korean medicine for the treatment of vascular diseases such as hypertension. The crude extract of EO contains phenolic compounds that are effective in protecting liver microsomes, hepatocytes, and erythrocytes against oxidative damage. But EO has been little found to have an anti-inflammatory activity. We investigated anti-inflammatory activity of EO in RAW 264.7 cells and human umbilical vein endothelial cells (HUVECs). Methods : Cytotoxic activity of EO on RAW 264.7 cells was investigated by using 5-(3-caroboxymeth-oxyphenyl)-2H-tetra-zolium inner salt (MTS) assay. The nitric oxide (NO) production was measured by Griess reagent system. And proinflammatory cytokines were measured by ELISA kit. The levels of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression were measured by flow cytometer. Results : EO decreased LPS-induced NO production in RAW 264.7 cells. The inhibitory activity of EO on LPS-induced NO release is probably associated with suppressing TNF-${\alpha}$, IL-6 and MCP-1 formation. These results indicate that EO has potential as an anti-inflammatory agent. Moreover, EO decreased TNF-${\alpha}$-induced IL-8, IL-6 production, and ICAM-1 and VCAM-1 expression in HUVECs. Conclusions : EO inhibits TNF-${\alpha}$-induced inflammation via decreasing cytokines production and adhesion molecules expression. These results indicate that EO has potential as an anti-inflammation and anti-artherosclerosis agent.

• Journal of Ginseng Research
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• 제44권4호
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• pp.593-602
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• 2020

Background: Heat stress orchestrates neurodegenerative disorders and results in the formation of reactive oxygen species that leads to cell death. Although the immunomodulatory effects of ginseng are well studied, the mechanism by which ginseng alleviates heat stress in the brain remains elusive. Methods: Rats were exposed to intermittent heat stress for 6 months, and brain samples were examined to elucidate survival and antiinflammatory effect after Korean Red Ginseng (KRG) treatment. Results: Intermittent long-term heat stress (ILTHS) upregulated the expression of cyclooxygenase 2 and inducible nitric oxide synthase, increasing infiltration of inflammatory cells (hematoxylin and eosin staining) and the level of proinflammatory cytokines [tumor necrosis factor α, interferon gamma (IFN-γ), interleukin (IL)-1β, IL-6], leading to cell death (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay) and elevated markers of oxidative stress damage (myeloperoxidase and malondialdehyde), resulting in the downregulation of antiapoptotic markers (Bcl-2 and Bcl-x_L) and expression of estrogen receptor beta and brain-derived neurotrophic factor, key factors in regulating neuronal cell survival. In contrast, KRG mitigated ILTHS-induced release of proinflammatory mediators, upregulated the mRNA level of the antiinflammatory cytokine IL-10, and increased myeloperoxidase and malondialdehyde levels. In addition, KRG significantly decreased the expression of the proapoptotic marker (Bax), did not affect caspase-3 expression, but increased the expression of antiapoptotic markers (Bcl-2 and Bcl-x_L). Furthermore, KRG significantly activated the expression of both estrogen receptor beta and brain-derived neurotrophic factor. Conclusion: ILTHS induced oxidative stress responses and inflammatory molecules, which can lead to impaired neurogenesis and ultimately neuronal death, whereas, KRG, being the antioxidant, inhibited neuronal damage and increased cell viability.

• Molecules and Cells
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• 제37권6호
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• pp.487-496
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• 2014

Angiotensinogen (AGT), the precursor of angiotensin I, is known to be involved in tumor angiogenesis and associated with the pathogenesis of coronary atherosclerosis. This study was undertaken to determine the role played by AGT in endothelial progenitor cells (EPCs) in tumor progression and metastasis. It was found that the number of EPC colonies formed by AGT heterozygous knockout ($AGT^{+/-}$) cells was less than that formed by wild-type (WT) cells, and that the migration and tube formation abilities of $AGT^{+/-}$ EPCs were significantly lower than those of WT EPCs. In addition, the gene expressions of vascular endothelial growth factor (VEGF), Flk1, angiopoietin (Ang)-1, Ang-2, Tie-2, stromal derived factor (SDF)-1, C-X-C chemokine receptor type 4 (CXCR4), and of endothelial nitric oxide synthase (eNOS) were suppressed in $AGT^{+/-}$ EPCs. Furthermore, the expressions of hypoxia-inducible factor (HIF)-$1{\alpha}$and $-2{\alpha}$ were downregulated in $AGT^{+/-}$ early EPCs under hypoxic conditions, suggesting a blunting of response to hypoxia. Moreover, the activation of Akt/eNOS signaling pathways induced by VEGF, epithelial growth factor (EGF), or SDF-$1{\alpha}$ were suppressed in $AGT^{+/-}$ EPCs. In $AGT^{+/-}$ mice, the incorporation of EPCs into the tumor vasculature was significantly reduced, and lung tumor growth and melanoma metastasis were attenuated. In conclusion, AGT is required for hypoxia-induced vasculogenesis.

• Journal of Ginseng Research
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• 제37권2호
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• pp.187-193
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• 2013

The effect of Korean red ginseng (KRG) on diabetic renal damage was investigated using streptozotocin (STZ)-induced diabetic rats. The diabetic rats showed loss of body weight gain, and increases in kidney weight and urine volume, whereas the oral administration of KRG at a dose of 100 or 250 mg/kg of body weight per day for 28 d prevented these diabetes-induced physiological abnormalities. Among the kidney function parameters, elevated plasma levels of urea nitrogen and creatinine in diabetic control rats tended to be lowered in KRG-treated rats. In addition, administration of KRG at a dose of 100 mg/kg body weight in the diabetic rats showed significant decreases in serum glucose and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), implying that KRG might prevent the pathogenesis of diabetic complications caused by impaired glucose metabolism and oxidative stress. KRG also significantly reduced advanced glycation end product (AGE) formation and secretion from kidney of diabetic rats. Furthermore, KRG decreased the levels of N-(carboxymethyl) lysine and expression of AGE receptor. KRG also reduced the overexpression of cyclooxygenase-2 and inducible nitric oxide synthase in the kidney via deactivation of nuclear factor-kappa B. We also found that KRG prevented STZ-induced destruction of glomerular structure and significantly suppressed high glucose-induced fibronectin production. Taken together, KRG ameliorates abnormalities associated with diabetic nephropathy through suppression of inflammatory pathways activated by TNF-${\alpha}$ and AGEs. These findings indicate that KRG has a beneficial effect on pathological conditions associated with diabetic nephropathy.