Journal
ARCHIVES OF PHARMACAL RESEARCH
Volume 34, Issue 5, Pages 791-800Publisher
PHARMACEUTICAL SOC KOREA
DOI: 10.1007/s12272-011-0513-5
Keywords
Chelerythrine chloride; Proliferation; Apoptosis; Human hepatoma SMMC-7721; Mitochondrial pathway; Bcl-2 family proteins
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Funding
- China Postdoctoral Science Foundation [20080430283]
- Jiangxi Yongfeng Boyuan Industry Co., Ltd.
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The objective of this study was to evaluate the antitumor activity of chelerythrine chloride (CHE) and investigate its potential apoptotic induction mechanism in SMMC-7721 cells. Our results suggested that the proliferation of SMMC-7721 cells was inhibited by CHE in a time and dose dependent manner, with a significant accumulation in S phase, and the cells exhibited typical apoptotic features. Moreover, CHE remarkably induced apoptosis by disruption of the mitochondrial membrane potential, release of Cyt-c, activation of caspase-3, and cleavage of poly-ADP-ribose polymerase in a dose dependent manner. Furthermore, the expression of Bcl-xl was downregulated while Bax and Bid expression was upregulated, and no variation was found for Bcl-2. These results indicated that CHE may play an important role in suppression of tumor growth by inducing apoptosis in human hepatoma cells via the activation of a mitochondrial pathway and regulating the expression of Bcl-2 family proteins.
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