INHIBITION OF TNF-α AND IL-6 PRODUCTION BY AUCUBIN THROUGH BLOCKADE OF NF-κB ACTIVATION IN RBL-2H3 MAST CELLS

Jeong, Hyun‐Ja; Koo, Hyun‐Na; Na, Ho-Jeong; Kim, Mi-Sun; Hong, Seung‐Heon; Eom, Jung-Woo; Kim, Kyung-Suk; Shin, Tae‐Yong; Kim, Hyung-Min

doi:10.1006/cyto.2002.0894

Cited by 150 publications

(86 citation statements)

References 41 publications

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“…29,30) Aucubin also inhibited IgE-induced TNF-a and IL-6 production via preventing nuclear factor-kB activity. 20) The spectrum of cytokines produced by HMC-1 cells with PMA plus A23187 stimulation supports the well-recognized role of mast cells immediate hypersensitivity. The present study reports inhibition of histamine and inflammatory production by Columbianetin on HMC-1 cells for the first time.…”

Section: Discussionsupporting

confidence: 52%

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Anti-inflammatory Effect of Columbianetin on Activated Human Mast Cells

Jeong

Kim

et al. 2009

Biological & Pharmaceutical Bulletin

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The inflammatory processes are orchestrated by inflammatory cells through a complex set of chemical signals and can arise in any tissue in response to traumatic, infectious, postischemic, toxic, allergic, or auto-immune injury. 1) In chronic inflammatory diseases, the injury persists and leads to tissue damage.1) During inflammation, the inflammatory region is infiltrated with mononuclear cells, producing a range of inflammatory mediators, including inflammatory cytokines. 2)Mast cells are widely distributed in the connective tissues of mammals and other vertebrates, where they are frequently located in close proximity to blood vessels.3) Mast cells are important effecter cells in allergic reactions as well as in inflammatory processes due to their ability to secrete numerous cytokines. 4,5) In view of such findings, the versatile role played by mast cells is now recognized, especially in allergic inflammation.6,7) Activated mast cells can produce histamine, as well as a wide variety of other inflammatory mediators such as eicosanoids, proteoglycans, proteases, and several proinflammatory and chemotactic cytokines such as tumor necrosis factor (TNF)-a, interleukin (IL)-1, IL-4, IL-6, IL-8, IL-13, and transforming growth factor (TGF)-b1. [8][9][10] Notably, modulation of the production of cytokines from mast cells can provide a useful therapeutic strategy for allergic inflammatory disease.In recent years, cyclooxygenase (COX)-2 plays important roles in various tumors and inflammatory diseases.11) COX-2, one of the major mediators of the inflammatory reactions, is also strongly induced in activated monocytes and macrophages. Several recent studies demonstrated that prostaglandin D2 (PGD2), the COX-2 metabolite released from activated mast cells, is also essential for the pathogenesis of eosinophilic airway inflammations.12) Previously, it has been reported that COX-2 inhibitors abolished the PGD2 synthesis and attenuated eosinophils accumulation in the airway's inflammations. 13)Corydalis heterocarpa has been used traditionally to treat the boil or dysentery as well as a poison in Korea. In this study, Columbianetin was isolated from Corydalis heterocarpa but its molecular mechanisms are not well understood. Ng et al., reported that Columbianetin inhibited lipid peroxidation in brain and kidney homogenates.14) It has been reported that one of the active compounds from roots of Angelica pubescens, Columbianetin acetate, significantly demonstrated anti-inflammatory and analgesic activities.15) Kang and Kim, reported that columbianetin-O-beta-D-glucopyranoside exhibited significant neuroprotective activities against glutamate-induced toxicity. 16)To investigate the effect of Columbianetin on phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore-induced cytokine production in the present study, we analyzed the production of IL-1b, IL-6, IL-8, and TNF-a on the Columbianetin treated human mast cell line, HMC-1. We also investigated the COX-2 expression by Columbianetin.Our results revealed that Columbianetin, the...

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Section: Discussionsupporting

confidence: 52%

“…19,20) IL-1b is a pro-inflammatory cytokine and a central mediator in the cytokine network, and is known to control important functions both in the immune system and inflammation. 21) TNF-a and IL-6 play major role in triggering and sustaining the inflammatory allergic response in mast cells.…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory Effect of Columbianetin on Activated Human Mast Cells

Jeong

Kim

et al. 2009

Biological & Pharmaceutical Bulletin

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“…Activation of the transcription factor NF-B has been implicated in the transcriptional regulation of TNF-␣ and IL-6 in a wide variety of systems (28,29). We therefore determined whether FC loading of macrophages leads to activation of the NF-B pathway.…”

Section: Fc Loading Of Macrophages Activates the Nf-b Pathway Which mentioning

confidence: 99%

Free Cholesterol-loaded Macrophages Are an Abundant Source of Tumor Necrosis Factor-α and Interleukin-6

Li¹,

Schwabe²,

DeVries-Seimon³

et al. 2005

Journal of Biological Chemistry

380

183

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Two key features of atherosclerotic plaques that precipitate acute atherothrombotic vascular occlusion ("vulnerable plaques") are abundant inflammatory mediators and macrophages with excess unesterified, or "free," cholesterol (FC). Herein we show that FC accumulation in macrophages leads to the induction and secretion of two inflammatory cytokines, tumor necrosis factor-␣ (TNF-␣) and interleukin-6 (IL-6). The increases in TNF-␣ and IL-6 mRNA and protein were mediated by FC-induced activation of the IB kinase/ NF-B pathway as well as activation of MKK3/p38, Erk1/2, and JNK1/2 mitogen-activated protein kinases (MAPK). Activation of IB kinase and JNK1/2 was needed for the induction of both cytokines. However, MKK3/p38 signaling was specifically involved in TNF-␣ induction, and Erk1/2 signaling was required for IL-6. Most interestingly, activation of all of the signaling pathways and induction of both cytokines required cholesterol trafficking to the endoplasmic reticulum (ER). The CHOP branch of the unfolded protein response, an ER stress pathway, was required for Erk1/2 activation and IL-6 induction. In contrast, one or more other ER-related pathways were responsible for activation of p38, JNK1/2, and IB kinase/NF-B and for the induction of TNF-␣. These data suggest a novel scenario in which cytokines are induced in macrophages by endogenous cellular events triggered by excess ER cholesterol rather than by exogenous immune cell mediators. Moreover, this model may help explain the relationship between FC accumulation and inflammation in vulnerable plaques.

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“…32) Previously, we reported that aucubin inhibited NF-kB activation via phosphorylation and degradation of IkB-a. 33) In this study, we showed that GJWGM suppresses NF-kB transcriptional activation and translocation to the nucleus induced by LPS in PBMC isolated from CI patients. This suppression is also mediated through the inhibition of IkB-a phosphorylation and degradation.…”

Section: Discussionmentioning

confidence: 68%

The Anti-inflammatory Effect of Gigukjiwhangwhangami through the Inhibition of Nuclear Factor-.KAPPA.B Activation in the Peripheral Blood Mononuclear Cells of Patients with Cerebral Infarction

Kim

Jeong

Moon

et al. 2006

Biological & Pharmaceutical Bulletin

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The Korean genuine medicine "Gigukjiwhangwhangami (GJWGM)" has long been used for various cerebrovascular diseases. However, the exact mechanism that accounts for the anti-inflammatory effect of GJWGM is not completely understood. The aim of the present study is to elucidate how GJWGM modulates the inflammatory reaction in lipopolysaccaride (LPS)-stimulated peripheral mononuclear cells from patients with cerebral infarction. Production of cytokine was measured by the ELISA and RT-PCR method. The level of nuclear factorkappaB (NF-k kB)/Rel A protein and NF-k kB DNA binding activity were determined by the Western blot analysis and TF-EIA method. We showed that GJWGM inhibited the production of tumor necrosis factor (TNF)-a a, interleukin (IL)-1a a, IL-6, and IL-8 induced by LPS in dose dependent manner (pϽ0.05). Maximal inhibition rate of TNF-a a, IL-1b b, IL-6 and IL-8 production by GJWGM was about 54.34%, 41.37%, 44.04%, and 54.46%, respectively. GJWGM inhibited the TNF-a a and IL-8 mRNA expression. In addition, we showed that the inhibitory mechanism of GJWGM is through the suppression of NF-k kB pathway. Our study suggests that an important molecular mechanism by GJWGM reduce inflammation, which may explain its beneficial effect in the regulation of inflammatory reactions.

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INHIBITION OF TNF-α AND IL-6 PRODUCTION BY AUCUBIN THROUGH BLOCKADE OF NF-κB ACTIVATION IN RBL-2H3 MAST CELLS

Cited by 150 publications

References 41 publications

Anti-inflammatory Effect of Columbianetin on Activated Human Mast Cells

Anti-inflammatory Effect of Columbianetin on Activated Human Mast Cells

Free Cholesterol-loaded Macrophages Are an Abundant Source of Tumor Necrosis Factor-α and Interleukin-6

The Anti-inflammatory Effect of Gigukjiwhangwhangami through the Inhibition of Nuclear Factor-.KAPPA.B Activation in the Peripheral Blood Mononuclear Cells of Patients with Cerebral Infarction

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