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All issues > Volume 51(3); 2008

Original Article
Korean J Pediatr. 2008;51(3):307-314. Published online March 15, 2008.
Capsaicin induced apoptosis and the enhanced anticancer effect of anticancer drugs in cancer cells
Sun Young SY Kim1, You Jin YJ Lee1, Eun Hye EH Park1, Ho Keun HK Yi2, Dae Sun DS Jo3, Jung Soo JS Kim3, Pyoung Han PH Hwang3
1Research Institute of Clinical Medicine, Chonbuk National University, Jeonju, Korea
2Department of Biochemistry, Chonbuk National University, Jeonju, Korea
3Department of Pediatrics, Chonbuk National University, Jeonju, Korea
Correspondence Pyoung Han PH Hwang ,Email: hwaph@chonbuk.ac.kr
Abstract
Purpose
: Capsaicin, the major pungent ingredient in red pepper, has long been used in spices and food additives. It has been recently shown to induce apoptosis in several cell lines through a not well known mechanism. The aim of this study was to investigate the apoptosis-inducing effect of capsaicin on gastric cancer cells, and to provide valuable information concerning the application of capsaicin for therapeutic purposes.
Methods
: Cultured SNU-668 cells were treated with capsaicin. We analyzed cell survival by trypan blue and crystal violet analysis, cell cytotoxicity by MTT assay, apoptosis by nuclear condensation and DNA fragmentation, bcl-2 and bax mRNA expression by RT-PCR, and the expression of apoptosis related proteins by Western immunoblot analysis. In order to assess whether the growth inhibitory effect of anticancer drugs is enhanced by capsaicin, we investigated the effects of cell cytotoxicity and the expression of apoptosis related proteins of etoposide and adriamycin treated with capsaicin in cells.
Results
: Capsaicin inhibited growth of SNU-668 cells in a dose-dependent manner. This inhibitory effect of capsaicin on cell growth was mainly due to the induction of apoptosis as evidenced by DNA fragmentation, nuclear condensation and the expression of apoptosis related proteins. Furthermore, capsaicin prominently reduced the ratio of anti-apoptotic Bcl-2 to pro-apoptotic Bax and consequently increased caspase-3 activity. The cells treated with capsaicin were more sensitive to death induced by etoposide and adriamycin than the cells without capsaicin.
Conclusion
: These results demonstrate that capsaicin efficiently induced apoptosis in SNU-668 cells through a caspase- 3-dependent mechanism and sensitizes cancer cells to anticancer drugs toward apoptotic cell death, which may contribute to its anticancer effect and chemosensitizer function against gastric cancer.

Keywords :Capsaicin, Apoptosis, Chemosensitivity, Gastric cancer

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