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Cannabidiol induced a contrasting pro-apoptotic effect between freshly isolated and precultured human monocytes.

Abstract

It has been documented that cannabidiol (CBD) induced apoptosis in a variety of transformed cells, including lymphocytic and monocytic leukemias. In contrast, a differential sensitivity between normal lymphocytes and monocytes to CBD-mediated apoptosis has been reported. The present study investigated the pro-apoptotic effect of CBD on human peripheral monocytes that were either freshly isolated or precultured for 72h. CBD markedly enhanced apoptosis of freshly isolated monocytes in a time- and concentration-dependent manner, whereas precultured monocytes were insensitive. By comparison, both cells were sensitive to doxorubicin-induced apoptosis. CBD significantly diminished the cellular thiols and glutathione in freshly isolated monocytes. The apoptosis induced by CBD was abrogated in the presence of N-acetyl-L-cysteine, a precursor of glutathione. In addition, precultured monocytes contained a significantly greater level of glutathione and heme oxygenase-1 (HO-1) compared to the freshly isolated cells. The HO-1 competitive inhibitor zinc protoporphyrin partially but significantly restored the sensitivity of precultured monocytes to CBD-mediated apoptosis. Collectively, our results demonstrated a contrasting pro-apoptotic effect of CBD between precultured and freshly isolated monocytes, which was closely associated with the cellular level of glutathione and the antioxidative capability of the cells.

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  • Publisher Full Text
  • Authors

    Wu HY, Chang AC, Wang CC, Kuo FH, Lee CY, Liu DZ, Jan TR

    Source

    Toxicology and applied pharmacology 246:3 2010 Aug 1 pg 141-7

    MeSH

    Acetylcysteine
    Antioxidants
    Apoptosis
    Cannabidiol
    Cells, Cultured
    Doxorubicin
    Glutathione
    Heme Oxygenase-1
    Humans
    Monocytes
    Protoporphyrins
    Sulfhydryl Compounds

    Pub Type(s)

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

    Language

    eng

    PubMed ID

    20471992