• 제목/요약/키워드: RAW 264.7 murine macrophage

검색결과 298건 처리시간 0.048초

미강에탄올추출물의 RAW264.7 세포에서 항염증효과 (Anti-Inflammatory Effects of Rice Bran Ethanol Extract in Murine Macrophage RAW 264.7 Cells)

  • 박정숙;김미혜
    • 약학회지
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    • 제55권6호
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    • pp.456-461
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    • 2011
  • The aim of the present study is to investigate the anti-inflammatory effect of a Rice Bran Ethanol Extract (RBE). Inflammation, such as a bacterial infection in vivo metabolites, such as external stimuli or internal stimuli to the defense mechanisms of the biological tissue a variety of intracellular regulatory factors deulin inflammatory TNF-${\alpha}$, IL-$1{\beta}$, IL-6, IL-8, such as proinflammatory cytokines, prostagrandin, lysosomal enzyme, free radicals are involved in a variety of mediators. The present study was designed to determine the effect of the RBE on pro-inflammatory factors such as NO, iNOS expression and TNF-${\alpha}$, IL-$1{\beta}$, IL-6 in lipopolysaccharide (LPS) - stimulated RAW264.7 macrophages cells. The cell toxicity was determined by MTS assay. To evaluate of anti-inflammatory effect of RBE, amount of NO was measured using the NO detection kit and the iNOS expression was measured by reverse transcriptase polymerase chain reaction (RT-PCR). And proinflammatory cytokines were measured by ELISA kit. As a result, the RBE reduced NO, iNOS expression and TNF-${\alpha}$, IL-$1{\beta}$, IL-6 production without cytotoxicity. Our results suggest that the RBE may have an anti-inflammatory property through suppressing inflammatory mediator productions and appears to be useful as an anti-inflammatory material.

Solanum nigrum L. Extract Inhibits Inflammation in Lipopolysaccharide-stimulated Raw 264.7 and BV2 Cells

  • Lee, Jin Wook;Jung, Hyuk-Sang;Sohn, Youngjoo;Kang, Yoon Joong
    • 한국자원식물학회:학술대회논문집
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    • 한국자원식물학회 2018년도 춘계학술발표회
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    • pp.92-92
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    • 2018
  • Solanum nigrum L. (SNL), generally known as black nightshade, is traditionally used as medicine to reduce inflammation caused by several diseases like asthma, chronic bronchitis and liver cirrhosis. In this study, anti-inflammatory effects of SNL extract were examined and possible molecular mechanisms of the anti-inflammatory effects were investigated. The inhibitory effects of SNL extract on nitric oxide (NO), pro-inflammatory cytokines ($TNF-{\alpha}$, IL-6) and Matrix metallopeptidase 9 (MMP-9) productions were dissected using lipopolysaccharide (LPS) stimulated murine macrophage-like cell line Raw264.7 cells and human microglial cell line BV2 cells. We further investigated whether SNL extract could suppress the phosphorylation of ERK1/2, JNK, and p38 and the nuclear expression of nuclear factor $NF-{\kappa}B$ p65 in LPS-stimulated Raw264.7 cells and BV2 cells. As a result, we showed that the SNL extract significantly decreased the production of pro-inflammatory cytokines, NO, and MMP-9. In addition, the SNL strongly inhibited the phosphorylation of ERK1/2, JNK, p38 and nuclear translocation of $NF-{\kappa}B$ p65 in activated cells. We confirmed that the extracts of SNL effectively inhibits the anti-inflammatory and may be used as a therapeutic to various inflammatory diseases.

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Anti-inflammatory Effects of Kochiae Fructus Extract on LPS-stimulated Raw 264.7 Cells

  • Kim, Bit-Na;Seong, Eun-Hwa;Kang, Yoon Joong
    • 한국자원식물학회:학술대회논문집
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    • 한국자원식물학회 2018년도 춘계학술발표회
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    • pp.90-90
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    • 2018
  • Kochiae Fructus is a medicinal plant used as medicine of the urinary organs, skin disease and inflammation. In this study, anti-inflammatory activity of Kochiae Fructus extract and its possible mechanisms of action were examined. The anti-inflammatory activity was investigated by inhibition of lipopolysaccharide (LPS) induced nitric oxide (NO), pro-inflammatory cytokine production and matrix metalloprotease-9 (MMP-9) in murine macrophage-like cell line Raw 264.7 cells. The measurement of the induced pro-inflammatory cytokine levels were carried out by ELISA. The phosphorylation of ERK1/2, JNK and MAPK and the nuclear expression of nuclear factor $NF-{\kappa}B$ p65 were investigated by Wesern blot analysis. The extract suppressed the phosphorylation of ERK1/2, JNK, and p38 MAPK, and the nuclear translocation of $NF-{\kappa}B$ p65 in activated cells. As a result, we suggest that the extract of Kochiae Fructus decreased the production of pro-inflammatory cytokines ($TNF-{\alpha}$, IL-6), nitric oxide, MMP-9 in LPS-induced Raw264.7 cells. Kochiae Fructus has possibility to be used as therapeutic benefits against inflammatory diseases.

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Suppressive Effect of Chlorella Methanol Extract on Oxidative Stress and NFkB Activation in RAW 264.7 Macrophages

  • Park, Ji-Young;Lee, Hyo-Sun;Song, Young-Sun
    • Preventive Nutrition and Food Science
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    • 제8권2호
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    • pp.124-129
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    • 2003
  • This study was designed to investigate whether a methanol extract of chlorella can suppress oxidative stress and nuclear factor kB (NFkB) activation in lipopolysaccharide (LPS)-stimulated RAW 264.7 murine macrophage cells. Treatment of RAW 264.7 cells with chlorella methanol extract (25, 50, and 100 $\mu$g/mL) significantly reduced LPS-stimulated nitric oxide production in a dose-dependent manner. Treatments with chlorella methanol extract at all concentrations also reduced thiobarbituric acid-reactive substances accumulation and enhanced glutathione level at 50 and 100 $\mu$g/mL levels. The specific DNA binding activities of NFkB on nuclear extracts in cells treated with 50 $\mu$g/mL and 100 $\mu$g/mL chlorella methanol extracts were significantly suppressed. These results suggest that chlorella methanol extract has mild antioxidative activity and the ability to suppress intracellular oxidative stress and NFkB activation.

Porphyromonas gingivalis의 각종 표면성분이 싸이토카인 형성에 미치는 영향 (The cytokine-inducing activities of surface components of the periodontopathogenic bacterium Porphyromonas gingivalis)

  • 김성조
    • Journal of Periodontal and Implant Science
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    • 제35권3호
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    • pp.799-811
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    • 2005
  • This study was carried out to examine the potency of the three surface compo- nents from Porphyromonas gingivalis to stimulate the murine macrophage cell line RAW264.7 to synthesize the pro-inflammatory cytokine tumor necrosis factor alpha($TNF-{\alpha}$) and nitric oxide (NO). Lipopolysaccharide(LPS). lipid A-associated proteins(LAP) and saline-extractable surface -associated material(SAM) were isolated from P. gingivalis 381. $TNF-{\alpha}$ release into culture supernatants was determined by two-site ELISA. NO production was assayed by measuring the accumulation of nitrite in culture supernatants. Western blot analysis of iNOS and analysis of reverse transcription(RT)-PCR products were carried out. The surface components extracted from this bacterium were almost equally potent in stimulating release of $TNF-{\alpha}$ and NO by RAW264.7 cells. $TNF-{\alpha}$ that was being measured immunologically was due to activation of $TNF-{\alpha}$ gene transcription. The present study clearly shows that P. gingivalis surface components fully induced iNOS expression in RAW264.7 cells in the absence of other stimuli. The ability of P. gingivalis surface components to promote the production of $TNF-{\alpha}$ and NO may be important in the pathogenesis of inflammatory periodontal disease.

Raloxifene, a Selective Estrogen Receptor Modulator, Inhibits Lipopolysaccharide-induced Nitric Oxide Production by Inhibiting the Phosphatidylinositol 3-Kinase/Akt/Nuclear Factor-kappa B Pathway in RAW264.7 Macrophage Cells

  • Lee, Sin-Ae;Park, Seok Hee;Kim, Byung-Chul
    • Molecules and Cells
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    • 제26권1호
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    • pp.48-52
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    • 2008
  • We here demonstrate an anti-inflammatory action of raloxifene, a selective estrogen receptor modulator, in lipopolysaccharide (LPS)-induced murine macrophage RAW264.7 cells. Treatment with raloxifene at micromolar concentrations suppressed the production of nitric oxide (NO) by down-regulating expression of the inducible nitric oxide synthase (iNOS) gene in LPS-activated cells. The decreased expression of iNOS and subsequent reduction of NO were due to inhibition of nuclear translocation of transcription factor NF-${\kappa}B$. These effects were significantly inhibited by exposure to the phosphatidylinositol 3-kinase (PI 3-kinase) inhibitor, LY294002, or by expression of a dominant negative mutant of PI 3-kinase. In addition, pretreatment with raloxifene reduced LPS-induced Akt phosphorylation as well as NF-${\kappa}B$ DNA binding activity and NF-${\kappa}B$-dependent reporter gene activity. Thus our findings indicate that raloxifene exerts its anti-inflammatory action in LPS-stimulated macrophages by blocking the PI 3-kinase-Akt-NF-${\kappa}B$ signaling cascade, and eventually reduces expression of pro-inflammatory genes such as iNOS.