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Bee venom protects hepatocytes from tumor necrosis factor-alpha and actinomycin D.

Abstract

Honeybee (Apis mellifera) venom (BV) has a broad array of therapeutic applications in traditional medicine to treat variety of diseases. It is also known that BV possesses anti-inflammatory and anticancer effect and that it can inhibit proliferation and induces apoptosis in cancer cells, but there is no evidence of information regarding anti-apoptosis of BV on hepatocytes. In the present study, we investigated the anti-apoptotic effect of BV on tumor necrosis factor (TNF)-alpha with actinomycin (Act) D induces apoptosis in hepatocytes. TNF-alpha/Act D-treated hepatocytes were exposed to different low concentration (1, 10 and 100 ng/mL) of BV. Our results showed statistically significant inhibition in DNA damage caused by BV treatment compared to corresponding TNF-alpha/Act D-treated hepatocytes. BV suppressed TNF-alpha/Act Dtreated activation of bcl-2 family and caspase family, which resulted in inhibition of cytochrome c release and PARP cleavage. These results demonstrate that low concentration BV possess a potent suppressive effect on anti-apoptotic responses of TNF-alpha/Act D-treated hepatocytes and suggest that these compounds may contribute substantial therapeutic potential for the treatment of liver diseases.

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  • Authors+Show Affiliations

    ,

    Department of Pathology, Catholic University of Daegu, College of Medicine, Daegu 705-718, Korea.

    , , , ,

    Source

    Archives of pharmacal research 33:2 2010 Feb pg 215-23

    MeSH

    Animals
    Apoptosis
    Bee Venoms
    Caspases
    Cell Line
    Cytochromes c
    DNA Fragmentation
    Dactinomycin
    Dose-Response Relationship, Drug
    Gene Expression Regulation
    Hepatocytes
    Mice
    Proto-Oncogene Proteins c-bcl-2
    Signal Transduction
    Tumor Necrosis Factor-alpha

    Pub Type(s)

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

    Language

    eng

    PubMed ID

    20195821