Capsaicin-induced Apoptosis in Human Hepatoma HepG2 Cells

  1. JAUNG-GENG LIN5
  1. 1Graduate Institute of Chinese Medical Science, Schools of Chinese Medicine, China Medical University, Taichung, Taiwan
  2. 2Department of Health Sciences, Chang Jung Christian University, Tainan, Taiwan
  3. 3Department of Food Nutrition, Chung-Haw University of Medical Technology, Tainan, Taiwan, R.O.C.
  4. 4Department of Biological Science and Technology, Schools of Chinese Medicine, China Medical University, Taichung, Taiwan
  5. 5Acupuncture Science, Schools of Chinese Medicine, China Medical University, Taichung, Taiwan
  1. Correspondence to: Jaung-Geng Lin, Chinese Medical Research Institute, China Medical University, No. 91, Hsueh-Shih Road, Taichung 404, Taiwan, R.O.C. Tel: +886 42205 33663311, Fax: +886 42203 5192, e-mail: jglin{at}mail.cmu.edu.tw

Abstract

Capsaicin, a pungent ingredient of red pepper, has been reported to possess antitumor activities. In this study, the effects of capsaicin on human HepG2 cells were investigated. Capsaicin reduced viability by PI incorporation in HepG2 cells in a dose and time dependent manner. Capsaicin promoted intracellular Ca2+ production and reactive oxygen species (ROS). The ΔΨm significantly decreased after capsaicin treatment for 24 h. Co-treatment of HepG2 cells with capsaicin and BAPTA (an intracellular Ca2+ chelator) significantly reduced intracellular Ca2+ levels, prevented ΔΨm disruption and inhibited apoptosis induction. The protein levels of Bcl-2 decreased and Bax increased in the mitochondrial fraction while the Bax protein decreased, and p53 and cytochrome c protein levels increased in the cytosolic fraction in HepG2 cells after capsaicin treatment for 24 h by Western blot. Immunostaining and confocal microscopic analysis also showed that capsaicin promoted cytoplasmic GADD153 expression and GRP78 nuclear translocation. The caspase-3 activity significantly increased after capsaicin treatment for 24 h. Our results indicated that the capsaicin-induced apoptosis in HepG2 cells may result from the elevation of intracellular Ca2+ production, ROS, disruption of ΔΨm, regulation of Bcl-2 family protein expression and caspase-3 activity.

Footnotes

    • Received April 8, 2008.
    • Revision received July 24, 2008.
    • Accepted November 3, 2008.
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    1. Anticancer Research vol. 29 no. 1 165-174
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