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The protective effect of bee venom against ethanol-induced hepatic injury via regulation of the mitochondria-related apoptotic pathway.

Abstract

Alcohol consumption increases apoptosis of hepatocytes. Death of hepatocytes is a characteristic feature of chronic liver disease for various causes. Bee venom (Apis mellifera) has been traditionally used for the treatment of various chronic diseases, such as chronic inflammatory arthritis and chronic liver disease. However, the precise mechanism for bee venom in chronic liver disease is not still cleared. To assess the effects of bee venom in chronic liver disease, we investigated the potential role of the bee venom in the ethanol-induced hepatocyte apoptosis. Bee venom treatment inhibited the apoptotic cell morphology and increased the cell viability in ethanol-induced hepatocyte apoptosis. With ethanol treatment, bee venom-treated hepatocytes increased activity of Bcl-2 and Bcl-xL, reduced activity of Bax, Caspase and PARP. In conclusion, bee venom treatment in ethanol-induced hepatocyte apoptosis occurred through the regulation of Bcl family with subsequent inactivation of the Caspase and PARP. These results suggest that bee venom could be an effective agent to reduce ethanol-induced hepatocyte apoptosis.

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  • Authors+Show Affiliations

    ,

    Department of Pathology, College of Medicine, Catholic University of Daegu, Daegu, Republic of Korea.

    , , , , , , ,

    Source

    MeSH

    Animals
    Apoptosis
    Bee Venoms
    Caspase Inhibitors
    Cell Line
    Cell Survival
    Cytoprotection
    Drug Antagonism
    Ethanol
    Fluorescent Antibody Technique, Indirect
    Hepatocytes
    Mice
    Mitochondria
    Poly(ADP-ribose) Polymerase Inhibitors
    Protective Agents
    Proto-Oncogene Proteins c-bcl-2
    bcl-2-Associated X Protein

    Pub Type(s)

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

    Language

    eng

    PubMed ID

    20210790

    Citation

    Kim, Kyung-Hyun, et al. "The Protective Effect of Bee Venom Against Ethanol-induced Hepatic Injury Via Regulation of the Mitochondria-related Apoptotic Pathway." Basic & Clinical Pharmacology & Toxicology, vol. 107, no. 1, 2010, pp. 619-24.
    Kim KH, Kum YS, Park YY, et al. The protective effect of bee venom against ethanol-induced hepatic injury via regulation of the mitochondria-related apoptotic pathway. Basic Clin Pharmacol Toxicol. 2010;107(1):619-24.
    Kim, K. H., Kum, Y. S., Park, Y. Y., Park, J. H., Kim, S. J., Lee, W. R., ... Park, K. K. (2010). The protective effect of bee venom against ethanol-induced hepatic injury via regulation of the mitochondria-related apoptotic pathway. Basic & Clinical Pharmacology & Toxicology, 107(1), pp. 619-24. doi:10.1111/j.1742-7843.2010.00549.x.
    Kim KH, et al. The Protective Effect of Bee Venom Against Ethanol-induced Hepatic Injury Via Regulation of the Mitochondria-related Apoptotic Pathway. Basic Clin Pharmacol Toxicol. 2010;107(1):619-24. PubMed PMID: 20210790.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - The protective effect of bee venom against ethanol-induced hepatic injury via regulation of the mitochondria-related apoptotic pathway. AU - Kim,Kyung-Hyun, AU - Kum,Yoon-Seup, AU - Park,Yoon-Yup, AU - Park,Ji-Hyun, AU - Kim,Soo-Jung, AU - Lee,Woo-Ram, AU - Lee,Kwang-Gil, AU - Han,Sang-Mi, AU - Park,Kwan-Kyu, Y1 - 2010/03/04/ PY - 2010/3/10/entrez PY - 2010/3/10/pubmed PY - 2010/10/13/medline SP - 619 EP - 24 JF - Basic & clinical pharmacology & toxicology JO - Basic Clin. Pharmacol. Toxicol. VL - 107 IS - 1 N2 - Alcohol consumption increases apoptosis of hepatocytes. Death of hepatocytes is a characteristic feature of chronic liver disease for various causes. Bee venom (Apis mellifera) has been traditionally used for the treatment of various chronic diseases, such as chronic inflammatory arthritis and chronic liver disease. However, the precise mechanism for bee venom in chronic liver disease is not still cleared. To assess the effects of bee venom in chronic liver disease, we investigated the potential role of the bee venom in the ethanol-induced hepatocyte apoptosis. Bee venom treatment inhibited the apoptotic cell morphology and increased the cell viability in ethanol-induced hepatocyte apoptosis. With ethanol treatment, bee venom-treated hepatocytes increased activity of Bcl-2 and Bcl-xL, reduced activity of Bax, Caspase and PARP. In conclusion, bee venom treatment in ethanol-induced hepatocyte apoptosis occurred through the regulation of Bcl family with subsequent inactivation of the Caspase and PARP. These results suggest that bee venom could be an effective agent to reduce ethanol-induced hepatocyte apoptosis. SN - 1742-7843 UR - https://www.unboundmedicine.com/medline/citation/20210790/The_protective_effect_of_bee_venom_against_ethanol_induced_hepatic_injury_via_regulation_of_the_mitochondria_related_apoptotic_pathway_ L2 - https://doi.org/10.1111/j.1742-7843.2010.00549.x DB - PRIME DP - Unbound Medicine ER -