• Journal of Microbiology and Biotechnology
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• v.18 no.12
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• pp.1984-1989
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• 2008

Surfactin is a natural biosurfactant derived from Bacillus subtilis and has various biological activities such as anticancer, antiplatelet, and anti-inflammatory effects. In this study, the inhibitory mechanism of surfactin in NO production from macrophages was examined. Surfactin down regulated LPS-induced NO production in RAW264.7 cells and primary macrophages with $IC_{50}$ values of 31.6 and $22.4{\mu}M$, respectively. Immunoblotting analysis showed that surfactin strongly blocked the phosphorylation of IKK and $l{\kappa}B{\alpha}$ and the nuclear translocation of $NF-{\kappa}B$ (p65). Therefore, these data suggest that surfactin may act as a bacterium-derived anti-inflammatory agent with anti-$NF-{\kappa}B$ activity.

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.2
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• pp.101-106
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• 2011

We demonstrate that glycoprotein isolated from Dioscorea batatas (GDB) has immunostimulatory effects including macrophage activation. Analysis of infiltration of inflammatory cells into peritoneal cavity showed GDB treatment significantly increased the recruitment of macrophages, lymphocytes, neutrophils, and monocytes into the peritoneal cavity. Treatment of spleen cells isolated from C57BL/6 mice with GDB significantly increased the proliferation of B cells and T cells induced by LPS and ConA, respectively. Treatment with GDB significantly increased the cytolytic capacity of NK cells and macrophages against YAC-1 and B16 cells, respectively. In order to further confirm and investigate the mechanism of GDB on macrophage activation, we analyzed the effects of GDB on the cytokine expression including iNOS, IL-1${\beta}$, and TNF-${\alpha}$ in mouse macrophage cell line, RAW 264.7 cells. RT-PCR and ELISA showed that GDB increased the expression of IL-1${\beta}$, and TNF-${\alpha}$, whereas iNOS was not induced by GDB. Collectively, this series of experiments indicates that GDB stimulates immune system including macrophage activation.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.3
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• pp.673-677
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• 2009

In order to verify the anti-inflammatory effects of Gelidium amansii, RAW264.7 macrophages were incubated with the extract of 70% ethanol solution (Ex), and activated with the endotoxin lipopolysaccharide (LPS). Ex inhibited the expression of the pro-inflammatory enzymes, including inducible nitric oxide (NO) synthase (iNOS) and cyclooxygenase-2 (COX-2), and the production of iNOS-mediated NO and COX-2-mediated prostglandin $E_2$ ($PGE_2$) production in a dose-dependent manner. Ex also reduced the release of the pro-inflammatory cytokines, including tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin-1${\beta}$ (IL-1${\beta}$) and IL-6 in LPS-activated macrophages, The observed anti-inflammatory effects of Ex was associated with inactivation of the nuclear factor ${\kappa}B$ (NF-${\kappa}B$) that mediates the induction of iNOS, COX-2, TNF-${\alpha}$, IL-1${\beta}$, and IL-6. Further studies showed that Ex inactivated NF-${\kappa}B$ through inhibition of phosphorylation of the inhibitory ${\kappa}B$ ($l{\kappa}B$), Taken together, these results suggest that Gelidium amansii exerts anti-inflammatory effects by inhibiting the expression of pro-inflammatory enzymes and the secretion of pro-inflammatory cytokines via inactivation of NF-${\kappa}B$ and/or $l{\kappa}B$.

• Natural Product Sciences
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• v.16 no.3
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• pp.153-158
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• 2010

To fine out the anti-inflammatory activities of the C. fragile. and its mechanism were investigated in macrophages induced by Peptidoglycan (PGN). Treatments of macrophages with 100 ug/ml of ethanol extract of Codium fragile (EECF) inhibited PGN-induced IL-6, NO and PGE2 production in a dose-dependent manner as well as expression of iNOS and COX-2. EECF inhibited PGN-induced extracellular signal-regulated kinase (ERK) 1/2, JNK 1/2 and p38 MAPK phosphorylation, which suggests that EECF inhibits IL-6 and NO secretion by blocking MAPKs phosphorylation. These findings may help elucidate the mechanism by which EECF modulates RAW 264.7 cell activation under inflammatory conditions.

• Journal of Photoscience
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• v.4 no.2
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• pp.31-34
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• 1997

The rapid and spontaneous interaction between superoxide anion radical and nitric oxide to yield the potent oxidants. peroxynitrite artion and peroxynitrous acid, was investigated in phorbol myristate acetate(PMA)-stimulated RAW264.7 macrophases by means of lucigenin- or luminol-enhanced chemiluminescence method. When RAW264.7 macrophages were stimulated by PMA. peroxynitrite-induced chemiluminescence was clearly observed. To prove observed chemiluminescencc due to the reaction between superoxide anion radical and nitric oxide produced by RAW264.7 macrophases, N-nitrosoglutathione (GSNO), a nitric oxide-releasing compound. superoxide dismutase(SOD), an enzyme removing superoxide anion radical by dismutating superoxide artion radical to hydrogen peroxide, and N-acethyl cysteine(NAC), a scarvenging reagent both superoxide artion radical and nitric oxide, were added in the cell system. Peroxynitrite- induced chemilumincscence was increased by exogenous addition of GSNO. whereas observed chemiluminescence was decreased by SOD and NAC. These results suggest that PMA-stimulated RAW264.7 macrophages produce both superoxide anion radical and nitric oxide to form peroxynitrite.

• Journal of Physiology & Pathology in Korean Medicine
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• v.22 no.2
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• pp.282-289
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• 2008

We evaluated the effect of SHBCS on adhesion and invasion of colon L5-26 adenocarcinoma cell line in vitro in vitro and experimental liver metastasis in vivo. SHBCS showed little inhibitory effect on colon 26-L5 cell proliferation. At the concentration of up to 500 mg/ml of SHBCS 80% of cells were viable. SHBCS showed no inhibitory effect on adhesion and invasion of colon 26-L5 cells, which were placed on matrigel. In a dose dependent manner, oral administration of SHBCS showed a significantly inhibitory effect on liver metastasis from colon 26-L5 injected mice. When mice were depleted of NK cells or macrophages before tumor inoculation, SHBCS significantly decreased liver metastasis fromf the tumor injected mice. Compared with the control mice, SHBCS increased the populations of macrophages and NK cells by 30%, 18%(10 mg/mouse, 50 mg/mouse) and 5%, 1% (10 mg/mouse, 50 mg/mouse) respectively. Compared with the control mice, SHBCS increased the populations of CD4 cells by 5%, 18% (10 mg/mouse, 50 mg/mouse) respectively. Spelenocytes from mice administerd with SHBCS were stimulated with LPS plus ConA, proliferation of splenocytes from mice administerd with SHBCS was 140%, 146%(10 mg/mouse, 50 mg/mouse) compared with th control mice. In conclusion, the present study suggests that SHBCS may have an inhibitory effect on liver metastasis through immunopotentiating activity which is associated with macrophages and NK cells.

• Parasites, Hosts and Diseases
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• v.39 no.1
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• pp.67-76
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• 2001

This experiment was focused on the characterization of anti- Toxoplasma monoclonal antibodies (mAbs) and the effect of mAbs on the parasite invasion of mouse peritoneal macrophages. Twenty eight mAbs including M110, M556, R7A6 and M62l were characterized by Ab titer, immunoglobulin isotyping and western blot pattern. Antibody titer (optical density) of 4 mAbs. Ml 10. M556. R7A6 and M62l. were 0.53,0.67, 0.45 and 0.39 (normal mouse serum; 0.19) with the same IgGl isotypes shown by Enzyme-linked immunosorbent assay (ELISA). Western blot analysis showed that Ml 10. M556. R7A6 and M62l reacted with the 33 kDa (p30),31 kDa (p28),43 kDa and 36 kDa protein. Immuno-gold labelling of mAbs M110, M556, R7A6 and M621 reacted with the surface membrane, dense granules and parasitophorous vacuolar membrane (PVM) , rhoptries and cytoplasm of tachyzoite, respectively. For in vitro assay, preincubation of tachyzoties with four mAbs, Ml 10, M556, R7A6 and M62l resulted in the decrease of the number of infected macrophages (p < 0.05) and the suppression of parasite multiplication at 18 h post-infection. Four monoclonal antibodies including Ml 10 (SAGI) were found to have an important role in the inhibition of macrophage invasion and T. gondii multiplication in vitro, and these mAbs may be suitable for vaccine candidates, diagnostic kit and for chemotherapy.

• Biomolecules & Therapeutics
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• v.16 no.4
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• pp.351-355
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• 2008

Prodigiosin was isolated from marine bacteria Hahella chejuensis which has been recently discovered from Marado, Cheju Island, Republic of Korea. Immunosuppressive properties have been reported for prodigiosin members such as undecylprodigiosin, metacycloprodigiosin, prodigiosin, and its synthetic analogue PNU156804 (PNU). However, the effect of this agent on the function of macrophage and splenocyte has not been characterized in detail. In the present study, we examined the effects of prodigiosin for its ability to alter the function of murine macrophage and NK cell, and the proliferation of splenocytes. When thioglycollate-elicited macrophages pre-exposed to prodigiosin (1-50 ng/ml) were stimulated with LPS/IFN-$\gamma$, pretreatment with prodigiosin resulted in the inhibition of tumoricidal activity of macrophage in a concentration-dependent manner. Tumoricidal activity of NK cell was also inhibited by prodigiosin. Moreover, we found that prodigiosin was able to cause a dose-dependent inhibition of murine lymphocyte responsiveness to Con A and LPS although T-mitogenic response was the more sensitive one. Taken together, the present results point out that prodigiosin has a suppressive effect on the mitogen-induced proliferation of murine lymphocytes and the function of macrophage and NK cell.

• Applied Microscopy
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• v.27 no.1
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• pp.31-46
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• 1997

Ultrastructure of mouse thymus was evaluated, following the administration of potassium dichromate and mercuric chloride, the heavy metals of evironmental pollutants. Potassium dichromate (20 mg/kg) or mercuric chloride solutions (10 mg/kg) were subcutanously injected to the mice. Six hours, three days and two weeks after the injections, animals were sacrificed. Thymic tissues were fixed in 2.5% glutaraldehyde-1.5% paraformaldehyde solutions. The procedure was followed by the fixation in 1% osmium tetroxide solutions. Washed and dehydrated tissue-blocks were embedded in the araldite mixture. Ultra-thin sections were stained with uranyl acetate-lead citrate solutions. Results observed were as follows: 1. In electron microscopy, cortical population of thymocytes in the thymus of experimental groups were reduced. especially in the outer cortex. Subcapsular cortices of potassium dichromate treated mice were filled with many epithelial reticular cells, whereas the similar area of mercuric chloride-treated mice exhibited large intercellular spaces. 2. In the thymus of mercuric chloride treated group, large intercellular spaces were formed by shrinkage of epithelial reticular cells, and the space was invaded by numerous cytoplasmic projections of macrophages. Thymocytes nuded out from the shrunken cytoplasm of epithelial reticular cells, presented numerous microvilli. 3. In the thymus of potassium dicromate treated group, many activated macrophages and plasma cells migrated into thymic cortices. 4. In the perivascular spaces of thymic cortices of potassium dichromate- and mercuric chloride-treated mice, activated macrophages. plasma cells, collagen fibrils, and flocculent substance of exudated materials were exhibited. From the above findifgs, it was concluded that potassium dichromate or mercuric chloride could disturb the normal differentiation or 'education' of T cells in the thymic cortex. In turn, these heavy metals may hurt the immunological defense mechanism.

• CELLMED
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• v.6 no.2
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• pp.13.1-13.7
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• 2016

Fatigue is a common complaint and affects the quality of life in modern people. Physical stress may induce activation of certain immune cells. Fermented porcine placenta (FPP) has been used to alleviate fatigue. Inflammatory cytokines are produced by physical stress and results in symptoms of fatigue. However, the role of FPP on fatigue-associated inflammatory cytokine production has not been elucidated yet. Thus, we estimated the anti-fatigue effect of FPP and its active components, leucine (Leu) and lysine (Lys) in activated RAW264.7 macrophages and forced swimming test (FST) fatigue animal model. Pretreatment with FPP, Leu, or Lys significantly inhibited the lipopolysaccharide (LPS)-induced tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 production without inducing cytotoxicity on LPS-stimulated RAW264.7 macrophages. FPP, Leu, or Lys inhibited the production of nitric oxide and downregulated the expression of inducible nitric oxide synthase on LPS-stimulated RAW264.7 macrophages. Furthermore, caspase-1 activities increased by LPS were significantly reduced by FPP, Leu, or Lys. In the FST, inflammatory cytokine levels of the mice administrated with FPP, Lys, and Leu were significantly reduced compared with the control group at 21 days. Collectively, these results show that anti-fatigue effect of FPP and its active components, Leu and Lys might be derived from the down-regulating of inflammatory mediators.