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Bee venom and melittin reduce proinflammatory mediators in lipopolysaccharide-stimulated BV2 microglia.

Abstract

Bee venom (BV), well known as a traditional Oriental medicine, has been shown to exhibit anti-arthritic and anti-carcinogenic effects. However, the molecular mechanisms responsible for the anti-inflammatory activity of BV have not been elucidated in microglia. In the present study, we investigated the anti-inflammatory effect of BV and its major component, melittin (MEL), on lipopolysaccharide (LPS)-stimulated BV2 microglia. Our results indicate that BV and MEL suppress LPS-induced nitric oxide (NO) and inducible NO synthase (iNOS) expression in a dose-dependent manner, without causing cytotoxicity in BV2 microglia. Moreover, BV and MEL suppressed LPS-induced activation of nuclear factor kappa B (NF-kappaB) by blocking degradation of IkappaBalpha and phosphorylation of c-Jun N-terminal kinase (JNK) and Akt, which resulted in inhibition of iNOS expression. Our data also indicate that BV and MEL exert anti-inflammatory effects by suppressing the transcription of cyclooxygenase (COX)-2 genes and proinflammatory cytokines, such as interleukin (IL)-1beta, IL-6 and tumor necrosis factor (TNF)-alpha. BV and MEL also attenuated the production of prostaglandin E(2) (PGE(2)). These results demonstrate that BV and MEL possess a potent suppressive effect on proinflammatory responses of BV2 microglia and suggest that these compounds may offer substantial therapeutic potential for treatment of neurodegenerative diseases that are accompanied by microglial activation.

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  • Authors+Show Affiliations

    ,

    Faculty of Applied Marine Science, Cheju National University, Jeju-si, Jeju Special Self-Governing Province 690-756, South Korea.

    , , , , , , ,

    Source

    International immunopharmacology 7:8 2007 Aug pg 1092-101

    MeSH

    Animals
    Antioxidants
    Bee Venoms
    Cell Line, Transformed
    Cell Survival
    Cyclooxygenase 2
    Dinoprostone
    Dose-Response Relationship, Drug
    Down-Regulation
    I-kappa B Kinase
    Immunoblotting
    Inflammation Mediators
    Interleukin-1beta
    Interleukin-6
    JNK Mitogen-Activated Protein Kinases
    Lipopolysaccharides
    Melitten
    Microglia
    NF-kappa B
    Nitric Oxide
    Nitric Oxide Synthase Type II
    Proline
    Proto-Oncogene Proteins c-akt
    RNA, Messenger
    Reverse Transcriptase Polymerase Chain Reaction
    Thiocarbamates

    Pub Type(s)

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

    Language

    eng

    PubMed ID

    17570326

    Citation

    Moon, Dong-Oh, et al. "Bee Venom and Melittin Reduce Proinflammatory Mediators in Lipopolysaccharide-stimulated BV2 Microglia." International Immunopharmacology, vol. 7, no. 8, 2007, pp. 1092-101.
    Moon DO, Park SY, Lee KJ, et al. Bee venom and melittin reduce proinflammatory mediators in lipopolysaccharide-stimulated BV2 microglia. Int Immunopharmacol. 2007;7(8):1092-101.
    Moon, D. O., Park, S. Y., Lee, K. J., Heo, M. S., Kim, K. C., Kim, M. O., ... Kim, G. Y. (2007). Bee venom and melittin reduce proinflammatory mediators in lipopolysaccharide-stimulated BV2 microglia. International Immunopharmacology, 7(8), pp. 1092-101.
    Moon DO, et al. Bee Venom and Melittin Reduce Proinflammatory Mediators in Lipopolysaccharide-stimulated BV2 Microglia. Int Immunopharmacol. 2007;7(8):1092-101. PubMed PMID: 17570326.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Bee venom and melittin reduce proinflammatory mediators in lipopolysaccharide-stimulated BV2 microglia. AU - Moon,Dong-Oh, AU - Park,Sung-Yong, AU - Lee,Kyeong-Jun, AU - Heo,Moon-Soo, AU - Kim,Ki-Cheon, AU - Kim,Mun-Ock, AU - Lee,Jae-Dong, AU - Choi,Yung Hyun, AU - Kim,Gi-Young, Y1 - 2007/05/02/ PY - 2007/02/24/received PY - 2007/04/06/revised PY - 2007/04/06/accepted PY - 2007/6/16/pubmed PY - 2007/10/25/medline PY - 2007/6/16/entrez SP - 1092 EP - 101 JF - International immunopharmacology JO - Int. Immunopharmacol. VL - 7 IS - 8 N2 - Bee venom (BV), well known as a traditional Oriental medicine, has been shown to exhibit anti-arthritic and anti-carcinogenic effects. However, the molecular mechanisms responsible for the anti-inflammatory activity of BV have not been elucidated in microglia. In the present study, we investigated the anti-inflammatory effect of BV and its major component, melittin (MEL), on lipopolysaccharide (LPS)-stimulated BV2 microglia. Our results indicate that BV and MEL suppress LPS-induced nitric oxide (NO) and inducible NO synthase (iNOS) expression in a dose-dependent manner, without causing cytotoxicity in BV2 microglia. Moreover, BV and MEL suppressed LPS-induced activation of nuclear factor kappa B (NF-kappaB) by blocking degradation of IkappaBalpha and phosphorylation of c-Jun N-terminal kinase (JNK) and Akt, which resulted in inhibition of iNOS expression. Our data also indicate that BV and MEL exert anti-inflammatory effects by suppressing the transcription of cyclooxygenase (COX)-2 genes and proinflammatory cytokines, such as interleukin (IL)-1beta, IL-6 and tumor necrosis factor (TNF)-alpha. BV and MEL also attenuated the production of prostaglandin E(2) (PGE(2)). These results demonstrate that BV and MEL possess a potent suppressive effect on proinflammatory responses of BV2 microglia and suggest that these compounds may offer substantial therapeutic potential for treatment of neurodegenerative diseases that are accompanied by microglial activation. SN - 1567-5769 UR - https://www.unboundmedicine.com/medline/citation/17570326/Bee_venom_and_melittin_reduce_proinflammatory_mediators_in_lipopolysaccharide_stimulated_BV2_microglia_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1567-5769(07)00107-5 DB - PRIME DP - Unbound Medicine ER -