• 고려인삼학회:학술대회논문집
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• 고려인삼학회 2006년도 춘계학술대회
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• pp.83-88
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• 2006

In this study we examined the potential for the synergistic augmentation of the activity of inflammatory mouse peritoneal macrophages by stimulation with RGAP combined with IFN-$\gamma$. The moderate augmentative effect induced by preincubation with RGAP was observed in the production of IL-1, IL-6 and NO but not TNF-$\alpha$. In addition, IFN-$\gamma$ had a low activating effect. Following preincubation with both RGAP A and IFN-$\gamma$, a marked enhancement of secretory activity and tumoricidal activity was noted in mouse peritoneal macrophages. Treatment of peritoneal macrophage with combination increased the generation of IL-1, IL-6, TNF-$\alpha$ and NO, whereas the production of reactive oxygen species were not altered. These results demonstrate the synergistic effects on macrophage function of RGAP in combination with IFN-$\gamma$ and suggest that the ability of IFN-$\gamma$ to prime macrophages to produce secretory molecules in response to RGAP may have implications for immunotherapy with this combination.

• 생약학회지
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• 제41권1호
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• pp.14-20
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• 2010

In this study, we investigated the anti-inflammatory effects of fupenjic acid (FA) isolated from the Potentilla discolor in both RAW 264.7 and mouse primary peritoneal macrophage cells. FA pretreatment significantly inhibited nitric oxide (NO) and prostaglandin $E_2(PGE_2)$ productions in the lipopolysaccharide (LPS)-induced RAW 264.7 and mouse primary peritoneal macrophage cells. Consistent with these observations, Western blot and RT-PCR analyses revealed that FA inhibited the LPS-induced expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the protein and mRNA levels. In addition, FA reduced the release of tumor necrosis factor-$\alpha$ (TNF-$\alpha$) and interleukin-6 (IL-6). These results suggest that the down regulation of iNOS and COX-2 expression and TNF-$\alpha$ and IL-6 production by fupenjic acid are responsible for its anti-inflammatory effects.

• 한국한의학연구원논문집
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• 제14권3호
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• pp.57-63
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• 2008

Glehnia littoralis (Umbelliferae) is the medicinal plant used traditionally for treatment of immune-related diseases. Prostaglandins and nitric oxide (NO) have been implicated as important mediators in the processes of inflammation and carcinogenesis. For understanding the mechanisms for pharmacological activities of Glehnia littoralis, we evaluated the inhibitory activity of Glehnia littoralis on lipopolysaccharide (LPS)-induced prostaglandin $E_2$ ($PGE_2$) and NO production in mouse macrophage RAW264.7 cells. The results showed that the extract of Glehnia littoralis inhibited LPS- induced $PGE_2$ production effectively, but not NO. Additional study revealed that the extract of Glehnia littoralis suppressed cyclooxygenase-2 (COX-2) expression in a dose-dependent manner. Present study suggests that Glehnia littoralis may have anti-inflammatory and/or cancer chemopreventive activity through the inhibition of $PGE_2$ production by the suppression of COX-2 activity.

• 한국식품영양학회지
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• 제21권2호
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• pp.204-209
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• 2008

The present study examined the ex vivo effect of Job's tear on immune function. Seven to eight week old mice(Balb/c) were fed a chow diet ad libitum two different concentrations (50 and 500 mg/kg BW) of water extract of Job's tear were orally administ every other day for two weeks. The results indicated that macrophage activation had occurred in the mice receiving 50 mg/kg B. W. of Job's tear water extract. Overall, using a mouse model, this study demonstrated that Job's tear extract may enhance immune function by regulating the $IL-1{\beta}$, IL-6, $TNF-{\alpha}$ and IL-10 cytokine production capacity of activated macrophages in mice. This study may suggest that supplementation of Job's tear water extracts may enhance the immune function by regulating the enhancing the cytokine production by activated macrophage ex vivo.

• 대한한의학회지
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• 제33권4호
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• pp.42-49
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• 2012

Objectives: The purpose of this study was to investigate effects of Red Ginseng-Ejung-tang Water Extract (ER) on cytokine production in RAW 264.7 mouse macrophages stimulated by lipopolysaccharide (LPS). Methods: Levels of various cytokines such as interleukin (IL)-6, IL-10, IL-2, IL-12p70, vascular endothelial growth factor (VEGF), monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)-2, keratinocyte-derived chemokine (KC), tumor necrosis factor (TNF)-alpha, granulocyte macrophage colony-stimulating factor (GM-CSF) were measured by high-throughput multiplex bead array cytokine assay based on xMAP (multi-analyte profiling beads) technology. Results: ER significantly decreased levels of IL-6, IL-10, IL-2, IL-12p70, VEGF, and MCP-1 for 24 hrs incubation at the concentrations of 25, 50, and $100{\mu}g/mL$ in LPS-induced RAW 264.7 cells (P < 0.05). But ER did not exert significant effects on production of MIP-2, KC, TNF-${\alpha}$, and GM-CSF in LPS-induced RAW 264.7 cells. Conclusions: These results suggest that ER has an anti-inflammatory property related with its inhibition of cytokine production in LPS-induced macrophages.

• 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.

• Archives of Pharmacal Research
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• 제22권3호
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• pp.267-273
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• 1999

In this study we examined the potential for the synergistic augmentation of the antitumor activity of inflammatory mouse peritoneal macrophages by stimulation with protein A combined with $IFN-\gamma$. The moderate augmentative effect induced by preincubation with protein A was demonstrated to be concentration-dependent, whereas IFN-, had a very low activating effect. Following preincubation with both protein A and $IFN-\gamma$, a marked enhancement of macrophage activity was noted. In addition, based on the utilization of neutralizing antibody to TNF-$\alpha$ or the inhibition of NO Production, TNF-$\alpha$ and NO were proven to be involved as mediators during the activation of tumoricidal macrophages by protein A in combination with $IFN-\gamma$. We also demonstrated that supernatants from macrophages treated with protein A plus $IFN-\gamma$ contained both TNF-$\alpha$ and NO at markedly increased levels. Thus, tumor cell lysis in the combined system was mediated via TNF-$\alpha$ or NO. These results demonstrate the synergistic effects on mouse pertioneal macrophage function of protein A in combination with $IFN-\gamma$ and suggest that combinations of such agents may serve as the basis for future in vivo immunotherapy.

• 동의생리병리학회지
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• 제23권5호
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• pp.1049-1054
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• 2009

The effect of Sacchromyces cerevisiae-Fermented Sophorae Radix water extract (SFS) on production of hydrogen peroxide and nitric oxide (NO) from mouse macrophage Raw 264.7 Cells treated with nicotine (1 mM) was investigated through this study. SFS (0, 25, 50, 100, 200, 400 ug/mL) was simultaneously treated with nicotine (1 mM) during culture of 4, 20, 24, 44, 48, 68, and 72 hr. And the intracellular productions of hydrogen peroxide were measured by dihydrorhodamine 123 (DHR) assay. NO production after 24 hr treatement was measured with Griess reagent assay. SFS restored the production of hydrogen peroxide and NO reduced by nicotine (1 mM) in Raw 264.7 Cells. These results suggests that SFS could be supposed to have the immunological activity concerned with macrophage's oxidative burst including hydrogen peroxide and NO.

• 동의생리병리학회지
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• 제23권4호
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• pp.883-887
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• 2009

The effects of Sacchromyces cerevisiae-Fermented Artemisiae Argi Folium Water extract (AFS) on Nitric oxide production from mouse macrophage Raw 264.7 cells treated with EtOH, gallic acid, Nicotine, Acetaminophen, and Acetaldehyde were investigated through this study. AFS (0, 10, 50, 100, 200, 400 ug/mL) was simultaneously treated with EtOH (100 uM), gallic acid (100 uM), Nicotine (1 mM), Acetaminophen (2 mM), and Acetaldehyde (200 uM). And Nitric oxide production from Raw 264.7 cells was measured by Griess reagent method. AFS restorated the cellular production of Nitric oxide reduced by EtOH, gallic acid, Nicotine, and Acetaminophen in Raw 264.7 cells. AFS could be supposed to have the immuno-modulating activity concerned with macrophage's production of Nitric oxide.

• 동의생리병리학회지
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• 제23권2호
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• pp.438-442
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• 2009

The purpose of this study is to investigate the effect of water extract from Artemisiae Argi Folium Fermented with Lactobacillus pentosus (AFL) on hydrogen peroxide production within mouse macrophage Raw 264.7 Cells treated with gallic acid, EtOH, Nicotine, Acetaminophen, and Acetaldehyde. AFL (0${\sim}$400 ug/mL) was treated with gallic acid, EtOH, Nicotine, Acetaminophen, and Acetaldehyde. And the intracellular productions of hydrogen peroxide were measured by dihydrorhodamine 123 (DHR) assay. AFL showed the restoration of the intracellular productions of hydrogen peroxide which were reduced by gallic acid, EtOH, Nicotine, Acetaminophen in Raw 264.7 Cells. AFL could be supposed to have the immunological activity related with macrophage's oxidative burst.