• Molecules and Cells
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• 제23권2호
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• pp.198-206
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• 2007

Hydroquinone is a toxic compound and a major benzene metabolite. We report that it strongly inhibits the activation of macrophages and associated cells. Thus, it suppressed the production of proinflammatory cytokines [tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-$1{\beta}$, IL-3, IL-6, IL-10, IL-12p40, IL-23], secretion of toxic molecules [nitric oxide (NO) and reactive oxygen species (ROS)] and the activation and expression of CD29 as judged by cell-cell adhesion and surface staining experiments. The inhibition was due to the induction of heme oxygenase (HO)-1 in LPS-activated macrophages, since blocking HO-1 activity with ZnPP, an HO-1 specific inhibitor, abolished hydroquinone's NO inhibitory activity. In addition, hydroquinone and inhibitors (wortmannin and LY294002) of the phosphatidylinositol-3 kinase (PI3K)/Akt pathway had very similar inhibitory effects on LPS-induced and CD29-mediated macrophage responses, including the phoshorylation of Akt. Therefore, our data suggest that hydroquinone inhibits macrophage-mediated immune responses by modulating intracellular signaling and protective mechanisms.

• 한국식품영양학회지
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• 제19권3호
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• pp.327-331
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• 2006

Zingiber officinale and Hizikia fusiforme(sea weed fusiforme) have long been used for food sources in Korea. The present study was performed to investigate the ex vivo effect of Zingiber officinale and Hizikia fusiforme on NO production in macrophage of mice. Seven to eight week old mices(Balb/c) were fed chew diet ad libitum and water extract of Zingiber officinale and Hizikia fusiforme was administrated orally at two different concentrations (50 and 500 mg/kg B.W.). every other day for two or four weeks NO(nitric oxide) production by activated macrophage was assessed by measuring nitrite, the stable NO metabolite, using Griess reaction assay. NO production were significantly enhanced in Zingiber officinale group at 500 mg/kg B.W. and in Hizikia fusiforme group at 50 mg/kg B.W. compared to the coresponding control groups. In conclusion, this study may suggest that Zingiber officinale and Hizikia fusiforme(sea weed fusiforme) extracts enhance the immune function by regulating NO production in macrophages of mice.

• 한국미생물·생명공학회지
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• 제22권2호
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• pp.182-189
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• 1994

The highest antitumor activity was observed in water soluble AS fraction of the Ganoderma lucidum IY 009. AS fraction did not show any cytotoxicity on sarcoma 180 cell but stimulated antibody production, opsonization of macrophage in ICR mouse and superoxide ion production from isolated macrophage. AS fraction activated complement C3 in human serum, and their antitumor activity was inhibited by EDTA, a chelator of cation related complementary activation. AS fraction exerted om prolong of life span and ingibition of tumor growth in the leukemia P388 or L1210 transplanted inbreed mouse,k BDF1 but krestin did not. AS fraction did not show any serious and lethal effects through oral administration on ICR mouse, and LD$_{50}$ of those was above 2,230 mg/kg.

• The Korean Journal of Physiology and Pharmacology
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• 제19권3호
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• pp.211-218
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• 2015

The present study showed that silymarin, a polyphenolic flavonoid isolated from milk thistle (Silybum marianum), inhibited lipopolysaccharide (LPS)-induced morphological changes in the mouse RAW264.7 macrophage cell line. We also showed that silymarin inhibited the nuclear translocation and transactivation activities of nuclear factor-kappa B (NF-${\kappa}B$), which is important for macrophage activation-associated changes in cell morphology and gene expression of inflammatory cytokines. BAY-11-7085, an NF-${\kappa}B$ inhibitor, abrogated LPS-induced morphological changes and NO production, similar to silymarin. Treatment of RAW264.7 cells with silymarin also inhibited LPS-stimulated activation of mitogen-activated protein kinases (MAPKs). Collectively, these experiments demonstrated that silymarin inhibited LPS-induced morphological changes in the RAW264.7 mouse macrophage cell line. Our findings indicated that the most likely mechanism underlying this biological effect involved inhibition of the MAPK pathway and NF-${\kappa}B$ activity. Inhibition of these activities by silymarin is a potentially useful strategy for the treatment of inflammation because of the critical roles played by MAPK and NF-${\kappa}B$ in mediating inflammatory responses in macrophages.

• BMB Reports
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• 제46권4호
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• pp.213-218
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• 2013

Members of the colony stimulating factor cytokine family play important roles in macrophage activation and recruitment to inflammatory lesions. Among them, granulocyte-macrophage colony stimulating factor (GM-CSF) is known to be associated with immune response to mycobacterial infection. However, the mechanism through which Mycobacterium tuberculosis (MTB) affects the expression of GM-CSF is poorly understood. Using PMA-differentiated THP-1 cells, we found that MTB infection increased GM-CSF mRNA expression in a dose-dependent manner. Induction of GM-CSF mRNA expression peaked 6 h after infection, declining gradually thereafter and returning to its basal levels at 72 h. Secretion of GM-CSF protein was also elevated by MTB infection. The increase in mRNA expression and protein secretion of GM-CSF caused by MTB was inhibited in cells treated with inhibitors of p38 MAPK, mitogen-activated protein kinase kinase (MEK-1), and PI3-K. These results suggest that up-regulation of GM-CSF by MTB is mediated via the PI3-K/MEK1/p38 MAPK-associated signaling pathway.

• 대한한의학회지
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• 제22권1호
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• pp.33-45
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• 2001

Objectives: This experimental study was carried out to prove the effect of Saenghyuldan(SHD; shengxiedan) on bone marrow failure induced by cyclophosphamide(CY) and irradiation in mice. Methods: The following were performed; immunopathology, histopathlogical findings of bone marrow and in the smear of myelocyte. hematopoietic cytokine(IL-3, GM-CSF, TPO), hematopoietic stem cell colony assay, humoral immunity(LPS mitogen response), cell-mediated immunity (Con A mitogen response) and nonspecific immunity(macrophage adherence & phagocytosis) in vitro or vivo. Results: SHD showed a protective effect on bone marrow failure induced by cyclophosphamide(CY) and irradiation in mice. SHD increased lymphoproliferative responses to LPS and Con A, and activated macrophage adherence and phagocytosis to SRBC. Conclusions: We expect that SHD can be used to treat bone marrow failure and immune suppression induced by the chemotherapy or radiation.

• 대한한의학회지
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• 제22권1호
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• pp.46-52
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• 2001

Objectives: This experimental study was carried out to evaluate the effects of PSM(polysaccharide of mushroom) on the immune activity. Methods: The following were performed; Immunotoxicity testing for immunopathology, IgO production & LPS mitogen response for humoral immunity, DTH, ConA mitogen response for cell-mediated immunity, and macrophage adherence & phagocytosis for nonspecific immunity in vitro or in vivo. Results: PSM showed a protective effect on cyclophosphamide-induced leukopenia, increased IgG production and lymphoproliferative responses to LPS; inhanced DTH and lymphoproliferative response Con A; and activated macrophage adherence and phagocytosis to SRBC. Conclusions: It is suggested that PSM can be used for cancer patients with immunosuppression and adapted to many other diseases.

• The Korean Journal of Physiology and Pharmacology
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• 제22권1호
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• pp.1-15
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• 2018

Inflammasomes are intracellular multiprotein complexes that coordinate anti-pathogenic host defense during inflammatory responses in myeloid cells, especially macrophages. Inflammasome activation leads to activation of caspase-1, resulting in the induction of pyroptosis and the secretion of pro-inflammatory cytokines including interleukin $(IL)-1{\beta}$ and IL-18. Although the inflammatory response is an innate host defense mechanism, chronic inflammation is the main cause of rheumatic diseases, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), ankylosing spondylitis (AS), and $Sj{\ddot{o}}gren^{\prime}s$ syndrome (SS). Since rheumatic diseases are inflammatory/autoimmune disorders, it is reasonable to hypothesize that inflammasomes activated during the inflammatory response play a pivotal role in development and progression of these diseases. Indeed, previous studies have provided important observations that inflammasomes are actively involved in the pathogenesis of inflammatory/autoimmune rheumatic diseases. In this review, we summarize the current knowledge on several types of inflammasomes during macrophage-mediated inflammatory responses and discuss recent research regarding the role of inflammasomes in the pathogenesis of inflammatory/autoimmune rheumatic diseases. This avenue of research could provide new insights for the development of promising therapeutics to treat inflammatory/autoimmune rheumatic diseases.

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.310.3-311
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• 2002

Macrophages have been known to play an essential role in tumor angiogenesis and produce a number of growth stimulators and inhibitors. Thus macrophages appear to influence every stage of angiogenesis. In this report, TNF-$\alpha$ was able to induce the production of IFN-${\gamma}$ in cancer cell-contanted macrophage. TNF-${\gamma}$ alone released relatively little IFN-${\gamma}$ whereas live tumor cells (3LL) alone releasd IFN-${\gamma}$ markedly from macrophage. (omitted)

• Parasites, Hosts and Diseases
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• 제52권6호
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• pp.695-699
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• 2014

Chronic Opisthorchis viverrini-induced hepatobiliary disease is associated with significant leukocyte infiltration, including activated macrophages; however, the polarization of infiltrating macrophages remains to be fully characterized. In this study, we characterized macrophage polarization and phenotype in chronic O. viverrini-induced hepatobiliary disease in humans and hamsters using gene expression and histochemical analysis. Chronic O. viverrini infection and associated hepatobiliary diseases were associated with iron loaded M2-like macrophages in both humans and hamsters. This study provides suggestive evidence that iron loaded M2-like macrophages promote hepatobiliary disease in chronic O. viverrini infection.