• Journal of Veterinary Clinics
• /
• v.21 no.1
• /
• pp.23-28
• /
• 2004

1,2-benzopyrone has been shown to affect on the activation and stimulation of macrophage. To examine the immunostimulating effect of 1,2-benzopyrone on the phagocytic response of canine peripheral blood mononuclear cells (PBMC) as well as polymorphonuclear cells (PMN), the phagocytic activity of phagocytes was analyzed by flow cytometry system using FITC-labelled latex. The 1,2-benzopyrone did not show any direct effect on phagocytic response of PBMC and PMN. But it showed an enhanced effect on the phagocytic response of monocyte-rich cells fractioned by cell size from dot plot profile in flowcytometric cytography of PBMC. The phagocytic activity of these cells was also enhanced by addition of culture supernatant from PBMC treated with 1,2-benzopyrone. Similarly, the phagocytic activity of PMN but not PBMC in the same procedures was enhanced by culture supernatant from PBMC treated with 1,2-benzopyrone. However, the culture supernatant from PMN treated with 1.2-benzopyrone did not show the enhancing effect on phagocytic activity for monocyte-rich cells and PMN. These results, therefore, suggested that enhanced phagocytic activity of canine peripheral blood PMN and monocytes may be mainly mediated by humoral factor(S) released from PBMC treated with 1,2-benzopyrone.

• Journal of the Korean Society of Food Culture
• /
• v.33 no.2
• /
• pp.104-111
• /
• 2018

This study aims to compare and analyze a willow tree (Salix Koreensis andersson) extract's antioxidant and anti-inflammatory activity by investigating its: total polyphenol, flavonoid content, SOD-like activity, DPPH vitality. the willow tree was induced with LPS to determine its active anti-inflammatory effects. as a result, the willow methanol extract showed a higher total polyphenol and flavonoid content than those of willow distilled water extract, but the willow distilled water extract showed a higher SOD than that of willow methanol extract. in its DPPH scavenging ability, the willow methanol extract's antioxidant activity was higher than that of the willow distilled water extract. the willow extract's measurements such as the production of NO, inflammatory cytokine ($TNF-{\alpha}$, IL-6 measurement) were significantly reduced as its concentration level went down. according to the research outcomes, when induced, he will extract's macrophage produces mediator-like substances such as NO and inflammatory cytokine that can be used to alleviate the inflammatory response. therefore, the willow tree proved to be a useful raw plant material for the products designed to combat inflammatory activities due to its natural antioxidant and anti-inflammatory response substances such as NO and cytokine.

• Archives of Pharmacal Research
• /
• v.25 no.2
• /
• pp.158-164
• /
• 2002

In the course of searching immunomodulators from natural sources, the protein-bound polysaccharide, CM-Ala, has been isolated from the water extract of Chelidonium majus L. (Papaveraceae). The immunostimulatory characteristics have been investigated in several experiments such as generation of activated killer (AK) cells, proliferation of splenocytes, activation of macrophages and granulocyte macrophage-colony forming cell (GM-CFC) assay. Of the fractions obtained using Sephacryl S200 column chromatography, CM-Ala was the most effective fraction that augmented the cytotoxicity against Yac-1 tumor cells from 0.88% to 34.18% by culturing with splenocytes for 5 days. CM-Ala also enhanced nitric oxide production by two fold in peritoneal macrophages and exhibited antitumor activity. It showed mitogenic activity on both spleen cells and bone marrow cells. CM-Ala induced proliferation of splenocytes by 84 fold and increased GM-CFC numbers by 1.48 fold over than the non-treated. On the contrary, CM-Ala had cytotoxic activity to a diverse group of tumor cells. From the above results, we proposed that CM-Ala has a possibility of an effective antitumor immunostimulator.

• Molecules and Cells
• /
• v.26 no.2
• /
• pp.193-199
• /
• 2008

The pro-apoptotic Bcl-2 family member Bim acts as a sensor for apoptotic stimuli and initiates apoptosis through the mitochondrial pathway. To identify novel regulators of Bim, we employed the yeast two-hybrid system and isolated the human gene encoding macrophage migration inhibitory factor (MIF), a ubiquitously expressed proinflammatory mediator that has also been implicated in cell proliferation, the cell cycle and carcinogenesis. The interaction between MIF and Bim was confirmed by both in vitro and in vivo protein interaction assays. Intriguingly, protein complexes between MIF and the three major Bim isoforms (BimEL/BimL/BimS) could be detected in HEK293 and K562 cells, especially in cells undergoing apoptosis. Moreover, exogenous expression of MIF partially inhibited Bim-induced apoptosis in HEK293 cells. SiRNA-mediated knockdown of MIF increased apoptosis in K562 cells exposed to the chemical oxidant diamide. Endogenous MIF may regulate the pro-apoptotic activity of Bim and inhibit the release of cytochrome c from mitochondria.

• Korean Journal of Food Science and Technology
• /
• v.50 no.5
• /
• pp.511-516
• /
• 2018

Macrophages play a crucial role in the host immune defense system. The current study investigated immunomodulatory activities induced by polysaccharides extracted from Cudrania tricuspidata (CTPS) fruits in murine macrophages and their role in signaling pathways. In macrophages, CTPS predominantly induced nitric oxide (NO), tumor necrosis factor-a, and interleukin-6 production. In addition, CTPS significantly up-regulated expression of the macrophage surface marker (CD80/86 and MHC class I/II). These results indicate that polysaccharides extracted from CTPS may potentially play an immunomodulatory role in macrophages via mitogen-activated protein kinases and nuclear factor-B signaling. These findings may be useful in the development of immune enhancing adjuvant materials obtained from natural sources.

• The Korean Journal of Physiology and Pharmacology
• /
• v.16 no.2
• /
• pp.131-138
• /
• 2012

Alcoholic hepatitis is a leading cause of liver failure in which the increased production of tumor necrosis factor ${\alpha}$ (TNF${\alpha}$) plays a critical role in progression of alcoholic liver disease. In the present study, we investigated the effects of cilostazol, a selective inhibitor of type III phosphodiesterase on ethanol-mediated TNF${\alpha}$ production in vitro and $in$ $vivo$, and the effect of cilostazol was compared with that of pentoxifylline, which is currently used in clinical trial. RAW264.7 murine macrophages were pretreated with ethanol in the presence or absence of cilostazol then, stimulated with lipopolysacchride (LPS). Cilostazol significantly suppressed the level of LPS-stimulated TNF${\alpha}$ mRNA and protein with a similar degree to that by pentoxifylline. Cilostazol increased the basal AMP- activated protein kinase (AMPK) activity as well as normalized the decreased AMPK by LPS. AICAR, an AMPK activator and db-cAMP also significantly decreased TNF${\alpha}$ production in RAW264.7 cells, but cilostazol did not affect the levels of intracellular cAMP and reactive oxygen species (ROS) production. The $in$ $vivo$ effect of cilostazol was examined using ethanol binge drinking (6 g/kg) mice model. TNF${\alpha}$ mRNA and protein decreased in liver from ethanol gavaged mice compared to that from control mice. Pretreatment of mice with cilostazol or pentoxifylline further reduced the TNF${\alpha}$ production in liver. These results demonstrated that cilostazol effectively decrease the ethanol-mediated TNF${\alpha}$ production both in murine macrophage and in liver from binge drinking mice and AMPK may be responsible for the inhibition of TNF${\alpha}$ production by cilostazol.

• The Korean Journal of Physiology and Pharmacology
• /
• v.21 no.5
• /
• pp.547-554
• /
• 2017

Previous studies have demonstrated the role of hydroquinone (HQ), a hydroxylated benzene metabolite, in modulating various immune responses; however, its role in macrophage-mediated inflammatory responses is not fully understood. In this study, the role of HQ in inflammatory responses and the underlying molecular mechanism were explored in macrophages. HQ down-regulated the expression of interferon $(IFN)-{\beta}$ mRNA in LPS-stimulated RAW264.7 cells without any cytotoxicity and suppressed interferon regulatory factor (IRF)-3-mediated luciferase activity induced by TIR-domain-containing adapter-inducing interferon-${\beta}$ (TRIF) and TANK-binding kinase 1 (TBK1). A mechanism study revealed that HQ inhibited IRF-3 phosphorylation induced by lipopolysaccharide (LPS), TRIF, and AKT by suppressing phosphorylation of AKT, an upstream kinase of the IRF-3 signaling pathway. IRF-3 phosphorylation is highly induced by wild-type AKT and poorly induced by an AKT mutant, AKT C310A, which is mutated at an inhibitory target site of HQ. We also showed that HQ inhibited IRF-3 phosphorylation by targeting all three AKT isoforms (AKT1, AKT2, and AKT3) in RAW264.7 cells and suppressed IRF-3-mediated luciferase activities induced by AKT in HEK293 cells. Taken together, these results strongly suggest that HQ inhibits the production of a type I IFN, $IFN-{\beta}$, by targeting AKTs in the IRF-3 signaling pathway during macrophage-mediated inflammation.

• Journal of the Society of Cosmetic Scientists of Korea
• /
• v.20 no.1
• /
• pp.25-36
• /
• 1994

It is weal known that bacterial lipopolysaccharide (LPS) stimulates prostaglandin synthesis in various experimental system via enhancing the expression of cylooxygenase-2 (COX-2). This study was designed to characterize U)5-induced prostaglandin synthesis in mouse peritoneal macrophages LPS-stimulated prostaglandin synthesis in macrophages with short term exposure was not so much prominent, but there was a burst in prostaglandin synthesis 8 hours after the LPS treatment and this u·as accompanied with the increase of cyclooxygenase activity, Dexamethasone markedly inhibited prostaglandin synthesis in this system. Metabolic label ins data supported above observations and thus, it could be concluded that LPS induces the do novo synthesis of COX-2 by which it stimulates the prostaglandin synthesis in mouse peritoneal macrophages, These data suggested that this experimental model system could be used for the screening procedure of COX-2 selective inhibitors. Ketoprofen, a non steroidal anti inflammatory agent, appeared to inhibit COX-1 relatively more selectively than COX-2.

• Korean Journal of Food Science and Technology
• /
• v.35 no.1
• /
• pp.132-137
• /
• 2003

Antioxidant and anti-inflammatory potentials of various grape extracts were evaluated. Extracts from Kyho seed, Kyho stem, and Campbell seed showed potent 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging activities compared to resveratrol $(IC_{50}=16.9,\;21.5,\;21.9,\;34.6\;{\mu}g/mL,\;respectively)$, among which, antioxidant effect of Kyho seed extract were similar to that of vitamin C $(IC_{50}=12.2\;{\mu}g/mL)$. These extracts also exhibited inhibitory activities on lipopolysaccharide (LPS)-induced prostaglandin $E_2$ production and nitrite formation in mouse macrophage RAW 264.7 cells at $50\;{\mu}g/mL$. Kyho stem and seed extracts showed growth inhibitory activities in human lung and colon cancer cells. These results suggest the potential roles of grape extracts as antioxidants and anti-inflammatory agents.

• The Journal of Korean Medicine
• /
• v.19 no.2
• /
• pp.485-501
• /
• 1998

Cortex Mori (Moros alba L.), the root bark of mulberry tree has been used as an autiphlogistic, diuretic and expectorant in herval medicine. Recently, a few papers reported that phenolic extract of Cortex Mori had the hypotensive, hypoglycemic, antiviral and anticancer effects, and hot water extract of Cortex Mori(CM) had inhibitory effect on the degranulation and histamine release from activated mast cells. These previous studies suggest a possibility that CM has an antidotal activity against inflammation which was mediated mainly by macrophage-secreting inflammatory factors. This study was performed to evaluate the influences of CM on carrageenan-induced edema in vivo and release of inflammatory mediators such as NO, TNF and IL-1 by macrophages stimulated with LPS or $IFN-{\gamma}$ in vitro. Subcutaneous injections of carrageenan into the mouse paw rapidly induced local edema by increasing vascular permeability, but single intraperitoneal injection of CM extract at 30 minutes before carrageenan suppressed the development of edema. NO and TNF production from macrophage stimulated by LPS or $IFN-{\gamma}$ were significantly suppressed, especially TNF secretion by up to 3-4 folds. LPS stimulated IL-1 production was also inhibited, but not significantly. Cell viability assay verified that the inhibition was not due to general cell toxicity. These results suggest that reduction of NO, TNF and IL-1 production may be one of the means by which CM prevent inflammation associated diseases.