Berberine, a Natural Product, Combined with Cisplatin Enhanced Apoptosis through a Mitochondria/Caspase-Mediated Pathway in HeLa Cells

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  • Youn Myung-Ja
    VestibuloCochlear Research Center and Department of Microbiology, Wonkwang University
  • So Hong-Seob
    VestibuloCochlear Research Center and Department of Microbiology, Wonkwang University
  • Cho Hea-Joong
    Department of Obstetrical & Gynecological Surgery, Wonkwang Medical Center, Wonkwang University
  • Kim Hyung-Jin
    VestibuloCochlear Research Center and Department of Microbiology, Wonkwang University
  • Kim Yunha
    VestibuloCochlear Research Center and Department of Microbiology, Wonkwang University
  • Lee Jeong-Han
    VestibuloCochlear Research Center and Department of Microbiology, Wonkwang University
  • Sohn Jung Sook
    VestibuloCochlear Research Center and Department of Microbiology, Wonkwang University
  • Kim Yong Kyu
    Department of Sports Sciences, College of Natural Sciences, Wonkwang University
  • Chung Sang-Young
    Department of Surgery, Chonnam National University Medical School
  • Park Raekil
    VestibuloCochlear Research Center and Department of Microbiology, Wonkwang University

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Berberine, a main component of Coptidis Rhizoma, has been extensively studied and is known to exhibit multiple pharmacologic activities. In this study, we investigated whether the combination of berberine and cisplatin exhibited significant cytotoxicity in HeLa cells. Apoptosis was evaluated based on DNA fragmentation and cytofluorometrically with the annexin-V/propidium iodide labeling method. Combined treatment with berberine and cisplatin acted in concert to induce loss of mitochondrial membrane potential (ΔΨm), release of cytochrome-c from mitochondria, and decreased expression of antiapoptotic Bcl-2, Bcl-x/L, resulting in activation of caspases and apoptosis. Further study showed that cell death induced by the combined treatment was associated with increased reactive oxygen species generation and lipid peroxidation. Moreover, we discovered that the combined treatment-induced apoptosis was mediated by the activation of the caspase cascade. These results indicated that the potential of cytotoxicity mediated through the mitochondria-caspase pathway is primarily involved in the combined treatment-induced apoptosis.

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