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Induction of apoptosis in human cervical carcinoma Hela cells with active components of Menispermum dauricum
Author(s) -
JawYuan Wang,
Shuqing Sun,
L Liu,
Wenji Yang
Publication year - 2014
Publication title -
genetics and molecular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.356
H-Index - 48
ISSN - 1676-5680
DOI - 10.4238/2014.february.13.17
Subject(s) - hela , apoptosis , flow cytometry , microbiology and biotechnology , immunocytochemistry , mtt assay , biology , caspase 3 , downregulation and upregulation , cell , programmed cell death , biochemistry , endocrinology , gene
Menispermum dauricum DC possesses a wide range of pharmacological effects. In this study, the mechanism of apoptosis induced by active components of M. dauricum was investigated in the human cervical carcinoma HeLa cell line. HeLa cells were treated with different M. dauricum concentrations over different time periods. The proliferation-inhibitory rate and cytotoxic effect of HeLa cells were measured by using the methyl thiazolyl tetrazolium (MTT) assay, and the apoptotic rate was detected by flow cytometry. Expressions of caspase-9, caspase-8, caspase-3, Bcl-2, and Fas proteins, in the apoptotic pathway, and the expression of nuclear factor-kappa B (NF-κB) were detected by SP immunocytochemistry. The MTT assay showed that active components of M. dauricum could significantly inhibit the growth of HeLa cells in a dose- and time-dependent manner (P<0.01). The Sub-Gl peak was found by flow cytometry, and the maximal apoptosis rate was 24.93%. Immunocytochemistry showed that after treatment with M. dauricum, the expressions of caspase-8, caspase-9, caspase-3, Fas protein, and NF-κB all increased, and the expression of the Bcl-2 protein decreased, with significant differences relative to the control group (P<0.01). Apoptosis in HeLa cells could be induced by active components of M. dauricum through the NF-κB signal transduction pathway and the caspase pathway, which was related to the downregulation of Bcl-2 expression and the upregulation of Fas expression.

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