Mitochondrial apoptosis induced by Chamaemelum nobile extract in breast cancer cells

Document Type: Research article

Authors

1 Physiology and Pharmacology Department, Pasteur Institute of Iran, Tehran, Iran

2 Ischemic Disorders Research Center, Golestan University of Medical Sciences, Gorgan, Iran

3 Center for Air Pollution Research (CAPR), Institute for Environmental Research(IER), University of Medical Sciences, Tehran, Iran

4 National Cell Bank of Pasteur Institute of Iran, Tehran, Iran.

Abstract

Chamaemelum nobile (Asteraceae) commonly known as 'Roman chamomile' is a medicinal plant used for numerous diseases in traditional medicine, although its anticancer activity is unknown. The present study was carried out to investigate the anticancer as well as apoptotic activity of ethyl acetate fraction of C. nobile on different cancerous cell lines. The cells were treated with varying concentrations (0.001- 0.25 mg/ml) of this fraction for 24, 48 and 72 h. Apoptosis induced in MCF-7 cells following treatment with ethyl acetate fraction was measured using Annexin V/PI, flowcytometry and western blotting analysis. The results showed that C. nobile ethyl acetate fraction revealed relatively high antiproliferative activity on MCF-7 cells; however, it caused minimal growth inhibitory response in normal cells. The involvement of apoptosis as a major cause of the fraction-induced cell death was confirmed by annexin- V/PI assay. In addition, ethyl acetate fraction triggered the mitochondrial apoptotic pathway by decreasing the Bcl-2 as well as increasing of Bax protein expressions and subsequently increasing Bax/Bcl-2 ratio. Furthermore, decreased proliferation of MCF-7 cells in the presence of the fraction was associated with G2/M phase cell cycle arrest.These findings confirm that ethyl acetate fraction of C.nobile may contain a diversity of phytochemicals which suppress the proliferation of MCF-7 cells by inducing apoptosis.

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Iranian Journal of Pharmaceutical Research

Volume 15, Special Issue
Winter 2016
Pages 197-204

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