Capsaicin-induced Apoptosis in Human Hepatoma HepG2 Cells

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Title:	Capsaicin-induced Apoptosis in Human Hepatoma HepG2 Cells
Authors:	(Shang-Pang Huang);陳榮洲(Jung-Chou Chen);(Chih-Chung Wu);(Chi-Tsai Chen);唐娜櫻(Nou-Ying Tang);(Yung-Tsuan Ho);(Chyi Lo);林景彬(Jing-Pin Lin);鍾景光(Jing-Gung Chung);林昭庚(Jaung-Geng Lin)
Contributors:	中醫學院學士後中醫學系學士班中醫內科學科
Keywords:	Capsaicin;calcium;reactive oxygen species;mitochondrial membrane potential;apoptosis;human HepG2 cells
Date:	2009.01
Issue Date:	2009-08-24 15:02:01 (UTC+8)
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.
Relation:	ANTICANCER RESEARCH 29(1 )165 ~174
Appears in Collections:	[Graduate Institute of Acupuncture Science] Journal articles

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