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Eryngium foetidum suppresses inflammatory mediators produced by macrophages.

Abstract

OBJECTIVE

This study assessed anti-inflammatory and antioxidant activities of E. foetidum leaf extract on LPS-activated murine macrophages.

METHODS

RAW264.7 cells were pretreated with or without E. foetidum extract for 1 h prior to incubation with LPS for 24 h. Anti-inflammatory activity was evaluated with reference to iNOS, COX-2, TNF-α and IL-6 gene expression. In addition, NO and intracellular ROS generation were determined by Griess method and fluorescence intensity and activation of MAPKs and IκB by Western blotting.

RESULTS

Prior treatment with E. foetidum leaf extract inhibited elevation of IL-6, TNF-α, iNOS and COX-2, together with their cognate mRNAs in a dose-dependent manner. NO and intracellular ROS contents were similarly reduced. These effects were due to inhibition of LPS-induced phosphorylation of JNK and p38 as well as IκB. E. foetidum ethanol extract was shown to contain lutein, β-carotenes, chlorogenic acid, kaempferol and caffeic acid, compounds known to exert these bioactive properties.

CONCLUSIONS

E. foetidum leaf extract possesses suppressive effects against pro-inflammatory mediators. Thus, E. foetidum has a high potential to be used as a food supplement to reduce risk of cancer associated with inflammation.

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    Source

    MeSH

    Animals
    Anti-Inflammatory Agents
    Antioxidants
    Apoptosis
    Blotting, Western
    Cell Proliferation
    Cells, Cultured
    Cyclooxygenase 2
    Enzyme-Linked Immunosorbent Assay
    Eryngium
    I-kappa B Proteins
    Inflammation
    Inflammation Mediators
    Interleukin-6
    Lipopolysaccharides
    Macrophages
    Mice
    Mitogen-Activated Protein Kinases
    NF-kappa B
    Nitric Oxide
    Nitric Oxide Synthase Type II
    Phosphorylation
    Plant Extracts
    Plant Leaves
    RNA, Messenger
    Reactive Oxygen Species
    Real-Time Polymerase Chain Reaction
    Reverse Transcriptase Polymerase Chain Reaction
    Signal Transduction
    Tumor Necrosis Factor-alpha

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    22524841

    Citation

    TY - JOUR T1 - Eryngium foetidum suppresses inflammatory mediators produced by macrophages. AU - Mekhora,Chusana, AU - Muangnoi,Channarong, AU - Chingsuwanrote,Pimjai, AU - Dawilai,Suwitcha, AU - Svasti,Saovaros, AU - Chasri,Kaimuk, AU - Tuntipopipat,Siriporn, PY - 2012/4/25/entrez PY - 2012/4/25/pubmed PY - 2012/9/21/medline SP - 653 EP - 64 JF - Asian Pacific journal of cancer prevention : APJCP JO - Asian Pac. J. Cancer Prev. VL - 13 IS - 2 N2 - OBJECTIVE: This study assessed anti-inflammatory and antioxidant activities of E. foetidum leaf extract on LPS-activated murine macrophages. METHODS: RAW264.7 cells were pretreated with or without E. foetidum extract for 1 h prior to incubation with LPS for 24 h. Anti-inflammatory activity was evaluated with reference to iNOS, COX-2, TNF-α and IL-6 gene expression. In addition, NO and intracellular ROS generation were determined by Griess method and fluorescence intensity and activation of MAPKs and IκB by Western blotting. RESULTS: Prior treatment with E. foetidum leaf extract inhibited elevation of IL-6, TNF-α, iNOS and COX-2, together with their cognate mRNAs in a dose-dependent manner. NO and intracellular ROS contents were similarly reduced. These effects were due to inhibition of LPS-induced phosphorylation of JNK and p38 as well as IκB. E. foetidum ethanol extract was shown to contain lutein, β-carotenes, chlorogenic acid, kaempferol and caffeic acid, compounds known to exert these bioactive properties. CONCLUSIONS: E. foetidum leaf extract possesses suppressive effects against pro-inflammatory mediators. Thus, E. foetidum has a high potential to be used as a food supplement to reduce risk of cancer associated with inflammation. SN - 1513-7368 UR - https://www.unboundmedicine.com/medline/citation/22524841/Eryngium_foetidum_suppresses_inflammatory_mediators_produced_by_macrophages_ L2 - http://www.apocpcontrol.org/page/apjcp_issues_view.php?sid=Entrez:PubMed&id=pmid:22524841&key=2012.13.2.653 ER -