• KSBB Journal
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• v.15 no.2
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• pp.156-161
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• 2000

This study was designed to investigate the antioxidative activity on oxidation of human low density lipoprotein(LDL) of band 2 fractionated from culture broth of Streptomyces sp. BH-405. Antioxidative activity of band 2 obtained from fractionation of BH-405 culture purification was measured against $Cu^{2+}$ mediated human LDL oxidation by thiobarbituric acid reactive substance. $CuSO_4$ mediated oxidation of LDL was degraded at a much higher rate than native LDL. Band 2 at a concentration of 100 or 200 !lg/mL inhibited the oxidation of LDL induced by $CuSO_4$, The formation of conjugated dienes induced in the presence of 5 !1M CuS04 of the mouse macrophage and J744. The electrophoretic mobility of the LDL in addition of $200\mu\textrm{g}$ band 2 in the presence of $5\mu\textrm{m}$ $CuSO_4$ was lower than that of native LDL. LDL modified by copper mediated or cell mediated uptake was degraded by macrophage at much greater than native LDL, and band 2 was found as potential inhibitor of modification of 125I-labelled LDL by macrophage. phage.

• IMMUNE NETWORK
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• v.14 no.4
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• pp.201-206
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• 2014

IL-33 is a member of the IL-1 cytokine family and plays a role in the host defense against bacteria, viruses, and fungi. In this study, we investigated the function of IL-33 and its receptor in in vitro macrophage responses to Candida albicans. Our results demonstrate that pre-sensitization of isolated peritoneal macrophages with IL-33 enhanced their pro-inflammatory cytokine production and phagocytic activity in response to C. albicans. These macrophage activities were entirely dependent on the ST2-MyD88 signaling pathway. In addition, pre-sensitization with IL-33 also increased ROS production and the subsequent killing ability of macrophages following C. albicans challenge. These results indicate that IL-33 may increase anti-fungal activity against Candida through macrophage-mediated resistance mechanisms.

• Korean Journal of Pharmacognosy
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• v.30 no.4
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• pp.363-367
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• 1999

Palmultang(PMT) consists of Ginseng Radix Alba, Atractylodis Rhizoma Alba, Hoelen, Glycyrrhizae Radix, Rehmanniae Radix Preparata, Paeoniae Radix, Cnidii Rhizoma and Angelicae Gigantis Radix. PMT enhanced the lucigenin chemiluminescence and the engulfment of fluorescein-conjugated E. coli particles and inhibited the production of nitric oxide in murine peritoneal macrophage. PMT enhanced the production of ${\gamma}-interferon$, interleukin-2 and the cell viability in murine thymocyte, but did not affect the production of interleukin-4. These results indicate that PMT enhances the phagocytosis of macrophage via the stimulation of ${\gamma}-interferon$ production in $T_H1$ cells and the reduction of nitric oxide production in peritoneal macrophage.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2010.06a
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• pp.280-280
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• 2010

Alzheimer disease is a progressive neurodegenerative disease of the aged, characterized by memory loss and dementia. For diagnosis of Alzheimer disease we have simply modified macrophage with amyloid beta bonded with different molecules. Modified Macrophage was observed with microscope for co-localization of amyloid beta molecule. For this experiment we used fluoroscene labeling substances. The macrophage was modified also with cell staining method. For cell staining method was used avidin-biotin reaction principles. All experiments were carried out on poly-L-lysine coated and sterilized glass substrates. In the presentation we will show the further investigations and applications with modified macrophage.

• Journal of Periodontal and Implant Science
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• v.23 no.1
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• pp.48-55
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• 1993

Macrophage inflammatory $protein-1{\alpha}(MIP-1{\alpha})$ from activated T cell or macrophage, which is small inducible cytokine of unkown biological function, has been shown to display inflammation chemokinetic activities, as well as myelosuppressive effect on more immature progenitor cells. In this paper we show the $MIP-1{\alpha}$ mRNA expression and the presence of $MIP-1{\alpha}$ binding sites from murine macrophage cell line RAW 264.7, and primary cells of mouse bone marrow and spleen. $MIP-1{\alpha}$ mRNA was induced from LPS-stimulated RAW 264.7, but not inhibited by cyclosporin A treatment, and also was expressed from mouse splenocyted and bone marrow cell which were not increased by ferritin or lactoferrin treatment. The results of receptor binding assay showed that radiolabeled RAW 264.7 cell with kd value of 0.91 nM, and binding sites per cell of 378. bone marrow cell and splenocyte also appeared to have $MIP-1{\alpha}$ binding sites 33 and 11 per cell, respectiviely.

• BMB Reports
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• v.50 no.10
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• pp.510-515
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• 2017

Triglyceride (TG) accumulation causes macrophage cell death, which affects the development of atherosclerosis. Here, we examined whether caspase-2 is implicated in TG-induced macrophage cell death. We found that caspase-2 activity is increased in TG-treated THP-1 macrophages, and that inhibition of caspase-2 activity drastically inhibits TG-induced cell death. We previously reported that TG-induced macrophage cell death is triggered by caspase-1, and thus investigated the relationship between caspase-2 and caspase-1 in TG-induced macrophage cell death. Inhibition of caspase-2 activity decreased caspase-1 activity in TG-treated macrophages. However, caspase-1 inhibition did not affect caspase-2 activity, suggesting that caspase-2 is upstream of caspase-1. Furthermore, we found that TG induces activation of caspase-3, -7, -8, and -9, as well as cleavage of PARP. Inhibition of caspase-2 and -1 decreased TG-induced caspase-3, -7, -8, and -9 activation and PARP cleavage. Taken together, these results suggest that TG-induced macrophage cell death is mediated via the caspase-2/caspase-1/apoptotic caspases/PARP pathways.

• Journal of Radiation Industry
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• v.4 no.3
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• pp.227-231
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• 2010

The purpose of this study was to investigate the expression mechanism of MCP-1 in gamma-irradiated RAW 264.7 macrophage cells. MCP-1 plays an important role in attracting monocyte to injured site at the early inflammation stage. However the production mechanism of MCP-1 by gamma-irradiation in RAW 264.7 macrophage cells was almost undiscovered. We found that MCP-1 was produced in RAW 264.7 macrophage cells by irradiation with 5 Gy. And these inceases were attenuated by specific inhibitors treatment, such as $NF-{\kappa}B$, JNK, ERK, JAK2, and Pyk2. These results indicate that radiation-induced MCP-1 production is mediated by MyD88- and TRIF-dependent pathways in RAW 264.7 macrophage cells. Furthermore, gamma-irradiation induced heme oxygenase-1 (HO-1) expression in RAW 264.7 macrophage cells. However this induction level was reduced before MCP-1 and $IFN-{\beta}$ production.

• Korean Journal of Food Science and Technology
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• v.31 no.5
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• pp.1363-1370
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• 1999

This study was performed to investigate the average molecular weight range of chitosan hydrolysates showing maximum effect in macrophage activation. Nitrite production by continuous macrophage cell line J774A.1 was the highest at $10\;{\mu}g/ml$ concentration of intact chitosan. Hydrogen peroxide production by J774A.1 showed the high value of $894\;{\mu}M/mg$ macrophage protein at $1,000\;{\mu}g/ml$ concentration of chitosan hydrolysate fraction 5 and $1,044\;{\mu}M/mg$ macrophage protein at $100\;{\mu}g/ml$ concentration of the fraction 6. Chitsan hydrolysate fraction 4, fraction 6 and intact chitosan enhanced $IL-1{\alpha}$ production, while the others did not. The production of tumor necrosis factor showed the high value at $1,000\;{\mu}g/ml$ concentration of chitosan hydrolysate fraction 4, $100\;{\mu}g/ml$ concentration of the fraction 5 and fraction 6, and $10\;{\mu}g/ml$ concentration of intact chitosan. In conclusion, fractions 4, 5 and 6 of the chitosan hydrolysatets with average molecular weight of $24,000{\sim}64,000$ calculated by HPLC analysis are the most effective in macrophage activation tested in this study.

• Journal of Life Science
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• v.18 no.6
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• pp.814-825
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• 2008

Ascochlorin (ASC) is prenyl-phenol compound that was isolated from the fungus Ascochyta viciae. ASC reduces serum cholesterol and triglyceride levels, and suppresses hypertension, tumor development, ameliorates type I and II diabetes. Here, to better understand the mechanisms by which ASC regulates physiological or pathological events and induces responses in the pharmacological treatment of inflammation, we performed differential analysis of the proteome of the mouse macrophage RAW264.7 cells in response to ASC. In this study, we used a proteomic analysis of LPS-induced RAW264.7 cells treated by ASC, to identify proteins potentially involved in inflammatory processes. The RAW264.7 cell proteomes with and without treatment with ASC were compared using two-dimensional electrophoresis (2-D SDS-PAGE), matrix-assisted laser desorption/ionization mass spectrometry (MALDI-TOF-MS) and bioinformatics. The largest differences in expression were observed for the calreticulin (4-fold decrease), ${\beta}-actin$ (4-fold decrease) and vimentin (1.5-fold decrease). In addition, rabaptin was increased 3-fold in RAW264.7 cells treated with ASC. The expression of some selected proteins was confirmed by RT-PCR analysis.

• Archives of Pharmacal Research
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• v.25 no.6
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• pp.895-902
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• 2002

Monocytes and macrophages playa major role in defense mechanism of the host response to tumor, in part through the secretion of several potent products and macrophage cytokines. Monocytes and tissue macro phages produce at least two groups of protein mediators of inflammation, interleukin 1 (IL-1) and tumor necrosis factor (TNF). Recent studies emphasizes that TNF and IL-1 modulate the inflammatory function of endothelial cells, leukocytes, and fibroblasts. In this study, our work is directed toward studying the in vitro effects of Korean propolis on the ability to induce cellular and secretory responses in murine macrophage cell line, RAW 264.7. It was found that Water Extract of Korean Propolis (WEP) could activate macro phages by producing cytokines. The production of the macrophage cytokines, IL-1 and TNF-$\alpha$, by RAW 264.7 treated with WEP was examined from 2.5 $\mu\textrm{g}$/ml up to 25 $\mu\textrm{g}$/ml with dose dependent manner. Nitric oxide (NO) production was also increased when cells were exposed to combination of LPS and WEP from 2.5 $\mu\textrm{g}$/ml up to 25 $\mu\textrm{g}$/ml. At high dose of WEP (50 to 100 $\mu\textrm{g}$/ml) used to prescribe for anti-inflammatory and analgesic medicine showed inhibition of NO production in LPS-stimulated macrophage. Besides cytokine production, NO release, surface molecule expression and cell morphologic antigen expression were increased in response to the stimulation by WEP. These results suggested WEP may function through macrophage activation.