• Title/Summary/Keyword: $TNF-{\alpha}$ release

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Study on Anti-allergic Effects of Electroacupuncture in Allergic Mouse Model

  • Yoon Ji-Won;Jeong Kyoung-Ah;Cho Zang-Hee;Sung Kang-Keyng
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.20 no.1
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    • pp.196-201
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    • 2006
  • Electroacupuncture(EA) is commonly used in various diseases. In the present study, the effect of EA in the allergic mouse model was examined. Allergy is generated via immunological mechanism and non-immunological mechanism. Mast cells activated dy those mechanisms get to release various substances such as histamine, leukotrienes, prostaglandin, TNF-$\alpha$, IL-4, IL-6, etc. which induce allergic reactions and the following inflammatory responses. To evaluate the anti-allergic effects of EA, mortality, ear swelling response, vascular permeability and cytokine secretion were investigated in EA group and non-EA group of which mice were compound 48/80-induced allergy model or PCA model. Compound 48/80 induces allergic reaction via non-immunological mechanism and PCA model is generated through the same mechanism with immediate-type(Type1) allergic reaction, one of immunological allergic reactions. EA inhibited compound 48/80-induced ear swelling response but did not inhibit the systemic anaphylaxis. EA also inhibited passive cutaneous anaphylaxis(PCA) activated dy anti-dinitrophenol IgE. In addition, EA inhibited IL-6 and TNF-$\alpha$ secretion from 48 h PCA in mice. These results indicate that EA may be used for the treatment of mast cell-mediated allergic diseases, especially immediate-type(Type 1) allergy and non-immunologically mediated allergy.

Comparison of Anti-allergenic Activities of Various Polyphenols in Cell Assays

  • Yun, Sang-Sik;Kang, Mi-Young;Park, Jun-Cheol;Nam, Seok-Hyun
    • Journal of Applied Biological Chemistry
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    • v.53 no.3
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    • pp.139-146
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    • 2010
  • The inhibitory effects of 25 polyphenols against in vitro allergic reactions were compared using biochemical and cell assays. Three polyphenols including curcumin, gallic acid, and quercetin suppressed the release of $\beta$-hexosaminidase from ionophore A23187-stimulated RBL-2H3 cells more effectively (>50% inhibition at $100{\mu}M$ concentration). They were found to have potencies in suppressing the release of histamine not only from ionophore A23187-, but also from immunoglobulin E (IgE)-stimulated RBL-2H3 cells. Moreover, such suppressive effects of the three polyphenols were also observed in A23187 plus PMA-costimulated rat peritoneal mast cells. The extent of inhibition were quantified as the respective polyphenol concentration that inhibit 50% ($IC_{50}$) of $\beta$-hexosaminidase or histamine release, showing an inhibition tendency with decreasing order of curcumin>gallic acid>quercetin. Down-regulation of $Ca^{2+}$ influx was suggested as the cause of the inhibition of $\beta$-hexosaminidase and histamine releases in these cells. The immune process inhibition was confirmed by the observed reduction in the gene expressions and release of pro-inflammatory cytokine tumor necrosis factor (TNF)-$\alpha$, interleukin (IL)-$1\beta$, and IL-4, due probably to antioxidant activity of the polyphenols. These findings illustrate that curcumin, gallic acid, and quercetin may be beneficial against allergic inflammatory diseases.

Extracts of Allium fistulosum Attenuates Pro-Inflammatory Action in the Lipopolysaccharide-Stimulated BV2 Microglia Cells (Lipopolysaccharide에 의한 BV2 세포의 염증 반응에 대한 파 추출물의 저해 활성)

  • Park, Shin-Hyoung;Kim, Jung-In;Jeong, Yong-Kee;Choi, Yung-Hyun
    • Journal of Life Science
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    • v.21 no.6
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    • pp.796-804
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    • 2011
  • Microglia are central nervous system (CNS)-resident professional macrophages that function as the principal immune cells responding to pathological stimulations in the CNS. Activation of microglia, induced by various pathogens, protects neurons and maintains homeostasis in the CNS, but severe activation causes inflammatory responses secreting various neurotoxic molecules such as nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$) and pro-inflammatory cytokines. Allium fistulosum, a member of the onion family, is mainly cultivated for consumption, as well as medicinal use in Oriental medicine. It has been reported that A. fistulosum has various biological effects such as anti-oxidant, anti-platelet aggregation, anti-fungus and anti-cholesterol synthesis, however there has been no research about the anti-inflammatory effects of A. fistulosum extracts. In this study, it was undertaken to explore the functions of A. fistulosum as a suppressor of neuronal inflammation by using BV2 microglia cells. As a result, it was found that four kinds of extracts of A. fistulosum effectively reduced the expressions of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) at both mRNA and protein levels, and also attenuated pro-inflammatory cytokines such as tumor necrosis alpha (TNF-${\alpha}$), interleukin-$1{\beta}$ (IL-$1{\beta}$) and interleukin-6 (IL-6) at the mRNA level in BV2 stimulated by lipopolysaccharide (LPS). In addition, the extracts of A. fistulosum attenuated the release of NO markedly, as well as resulting in slight decreases of TNF-${\alpha}$ and IL-6 production, the effects of which were most significant when treated with ethyl alcohol extract from the whole A. fistulosum. In conclusion, the data indicated that the anti-inflammatory actions of A. fistulosum against BV2 microglia cells is through the down-regulation of iNOS, COX2 and pro-inflammatory cytokines such as TNF-${\alpha}$ and IL-6, and these effects are expected to help in the protection of nerve tissues by suppressions of neuronal inflammation in various neurodegenerative diseases.

Regulatory Effect of Atopic Allergic Reaction by Carpopeltis affinis

  • Na, Ho-Jeong;Moon, Phil-Dong;Hong, Seung-Heon;Seo, Young-Wan;Kim, Hyung-Min
    • Proceedings of the PSK Conference
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    • 2003.04a
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    • pp.142.2-143
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    • 2003
  • We studied the effect of methanol extract of Carpopeltis affinis (CA) on atopic allergic reaction. CA dose-dependently inhibited interleukin (IL)-8 and tumor necrosis factor (TNF)-$\alpha$ secretion from the PMA- plus A23187- stimulated HMC-1. CA also dose-dependently inhibited the histamine and $\beta$-hexosaminidase release from mast cells. CA had no cytotoxic effect. (omitted)

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The Effect of Barbaloin on LPS-stimulated Inflammatory Reaction in Mice Peritoneal Macrophages

  • Jeon, Yong-Deok;Lee, Jong-Hyun
    • Korean Journal of Plant Resources
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    • v.30 no.3
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    • pp.280-286
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    • 2017
  • Barbaloin is a major component of Aloe vera, which has been used for a laxative. Also, barbaloin is C-glucoside of aloe emodin anthrone which is founded in Aloe vera. Barbaloin has varieties of pharmacological activity such as inhibitory effects on inflammation, histamine release, cancer and microbial infection. But the effect of barbaloin on lipopolysaccharide (LPS)-stimulated macrophages has not been understood. In this study, we evaluated the effects of barbaloin against LPS-stimulated production of nitric oxide (NO), inflammatory cytokines and MAPKs activation in macrophage. We treated barbaloin (0.1, 1, 10, $100{\mu}M$) in LPS-stimulated mice peritoneal macrophage. Our results showed that barbaloin significantly inhibited production of NO and cytokines of tumor necrosis factor $(TNF)-{\alpha}$, interleukin (IL)-6, interleukin $(IL)-1{\beta}$ in LPS-stimulated peritoneal macrophage. Moreover, barbaloin inhibited the phosphorylation of ERK and JNK in a dose dependent manner. These results indicated that barbaloin could be useful for inflammatory diseases.

Macrophage Activation by an Acidic Polysaccharide Isolated from Angelica Sinensis (Oliv.) Diels

  • Yang, Xingbin;Zhao, Yan;Wang, Haifang;Mei, Qibing
    • BMB Reports
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    • v.40 no.5
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    • pp.636-643
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    • 2007
  • This study was designed to identify and characterize the mechanism of macrophage activation by AAP, an acidic polysaccharide fraction isolated from the roots of Angelica sinensis (Oliv.) Diels. As a result, AAP significantly enhanced nitric oxide (NO) production and cellular lysosomal enzyme activity in murine peritoneal macrophages in vitro and in vivo. Furthermore, L-NAME, a specific inhibitor of inducible nitric oxide synthase (iNOS), effectively suppressed AAP-induced NO generation in macrophages, indicating that AAP stimulated macrophages to produce NO through the induction of iNOS gene expression and the result was further confirmed by the experiment of the increase of AAP-induced iNOS transcription in a dose-dependent manner. To further investigate, AAP was shown to strongly augment toll-like receptor 4 (TLR4) mRNA expression and the pretreatment of macrophages with anti-TLR4 antibody significantly blocked AAP-induced NO release and the increase of iNOS activity, and tumor necrosis factor-$\alpha$ (TNF-$\alpha$) secretion.

Inhibitory effects of oroxylin A on endothelial protein C receptor shedding in vitro and in vivo

  • Ku, Sae-Kwang;Han, Min-Su;Lee, Min Young;Lee, You-Mie;Bae, Jong-Sup
    • BMB Reports
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    • v.47 no.6
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    • pp.336-341
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    • 2014
  • Endothelial cell protein C receptor (EPCR) plays important roles in blood coagulation and inflammation. EPCR activity is markedly changed by ectodomain cleavage and release as the soluble EPCR. EPCR can be shed from the cell surface, which is mediated by tumor necrosis factor-${\alpha}$ converting enzyme (TACE). Oroxylin A (OroA), a major component of Scutellaria baicalensis Georgi, is known to exhibit anti-angiogenic, antiinflammation, and anti-invasive activities. However, little is known about the effects of OroA on EPCR shedding. Data showed that OroA induced potent inhibition of phorbol-12-myristate 13-acetate (PMA), tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-$1{\beta}$ and on cecal ligation and puncture (CLP)-induced EPCR shedding through suppression of TACE expression and activity. In addition, treatment with OroA resulted in reduced PMA-stimulated phosphorylation of p38, extracellular regulated kinases (ERK) 1/2, and c-Jun N-terminal kinase (JNK). These results demonstrate the potential of OroA as an anti-sEPCR shedding reagent against PMA and CLP-mediated EPCR shedding.

Fisetin Suppresses Macrophage-Mediated Inflammatory Responses by Blockade of Src and Syk

  • Kim, Jun Ho;Kim, Mi-Yeon;Kim, Jong-Hoon;Cho, Jae Youl
    • Biomolecules & Therapeutics
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    • v.23 no.5
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    • pp.414-420
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    • 2015
  • Flavonoids, such as fisetin (3,7,3',4'-tetrahydroxyflavone), are plant secondary metabolites. It has been reported that fisetin is able to perform numerous pharmacological roles including anti-inflammatory, anti-microbial, and anti-cancer activities; however, the exact anti-inflammatory mechanism of fisetin is not understood. In this study, the pharmacological action modes of fisetin in lipopolysaccharide (LPS)-stimulated macrophage-like cells were elucidated by using immunoblotting analysis, kinase assays, and an overexpression strategy. Fisetin diminished the release of nitric oxide (NO) and reduced the mRNA levels of inducible NO synthase (iNOS), tumor necrosis factor (TNF)-${\alpha}$, and cyclooxygenase (COX)-2 in LPS-stimulated RAW264.7 cells without displaying cytotoxicity. This compound also blocked the nuclear translocation of p65/nuclear factor (NF)-${\kappa}B$. In agreement, the upstream phosphorylation events for NF-${\kappa}B$ activation, composed of Src, Syk, and I${\kappa}B{\alpha}$, were also reduced by fisetin. The phospho-Src level, triggered by overexpression of wild-type Src, was also inhibited by fisetin. Therefore, these results strongly suggest that fisetin can be considered a bioactive immunomodulatory compound with anti-inflammatory properties through suppression of Src and Syk activities.

Effects of Interleukin-$1\beta$, Tumor Necrosis Factor-$\alpha$ and Interferon-$\gamma$ on the Nitric Oxide Production and Osteoclast Generation in the Culture of Mouse Bone Marrow Cells

  • Kwon, Young-Man;Kim, Se-Won;Ko, Seon-Yle
    • International Journal of Oral Biology
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    • v.31 no.2
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    • pp.67-72
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    • 2006
  • Nitric oxide(NO) is a labile, uncharged, reactive radical that functions as a sensitive mediator of intercellular communication in diverse tissues. It has been reported that NO is produced by osteoblast and these results may suggest that NO is integrally involved in the regulation of osteoclast formation and osteoclast resorption activity by osteoblastic cells. We examined the effect of cytokines on NO release by mouse bone marrow cell. We also examined the effects of cytokines and sodium nitroprusside(SNP) on the formation of osteoclast-like cell from mouse bone marrow cells in culture. Cytokines stimulated NO production of mouse bone marrow cells, and N-nitro-L-arginine methyl ester, a specific inhibitor of NO synthase, suppressed the cytokine-induced NO production. SNP showed dual action in the generation of osteoclasts. The addition of $30{\mu}M$ SNP inhibited the formation of tartrate resistant acid phosphatase(TRAP)(+) multinucleated cell, whereas lower concentration($3{\mu}M$) of SNP enhanced it. Although the precise action of NO remains to be elucidated in detail, the action of NO in osteoclast generation in our studies seems to be associated, at least in part, with bone metabolism and bone pathophysiology.

Germanium-Fortified Yeast Activates Macrophage, NK Cells and B Cells and Inhibits Tumor Progression in Mice. (게르마늄 강화효모의 마우스에서의 암세포 억제 및 대식세포, NK 세포, B 세포의 활성화에 관한 연구)

  • Baek, Dae-Heoun;Jung, Jin-Wook;Sohn, Tsang-Uk;Kang, Jong-Koo
    • Microbiology and Biotechnology Letters
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    • v.35 no.2
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    • pp.118-127
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    • 2007
  • Germanium-fortified yeast (GY) is a organic germanium-fortified yeast with potent immune modulating activities including anti-inflammatory effect. Through cell line studies, we observed that GY can modulate the diverse immune activity but little evidence was provided on the mechanism of GY in modulating immune activities in other higher animals. In this study, we investigated the effect of GY on modulation of immune function in mice. GY was administered in normal mice or tumor-bearing mice and then effect of GY on modulation of host immune system was analyzed by using ex vivo isolated macrophages, B cells, NK cells. Admistration of GY in mice induced macrophage activation thereby increased effector function of macrophage such as increased phagocytosis, chemotaxis, adherence, $O_2-release$, NO, $TNF-{\alpha}$ production. In addition, GY administration Increased B lymphocyte activation and plaque forming cells. Furthermore, GY administration increased NK-cell mediated cytotoxicity. Furthermore, GY administration suppressed progression of tumor in mice by increasing $TNF-{\alpha}$ production and effector function of NK cells. Our results showed that GY has a potent immunostimulatory function in vivo mice model. Proper modulation and administration of GY in human could be helpful to maintaining immunological homeostasis by modulating host immune system.