Active Fractions of Dichloromethane Extract of Artemisia Aucheri Inhibit Proliferation of Human Breast Cancer MCF-7 Cells via Induction of Apoptosis

Mahdi Mojarrab; Alireza Pourasadollah; Hajar Motamed; Farahnaz Ahmadi; Leila Hosseinzadeh; Marziyeh Hajialyani

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Active Fractions of Dichloromethane Extract of Artemisia Aucheri Inhibit Proliferation of Human Breast Cancer MCF-7 Cells via Induction of Apoptosis

Author(s):

Mahdi Mojarrab¹,

Alireza Pourasadollah¹,

Hajar Motamed¹,

Farahnaz Ahmadi¹,

Leila Hosseinzadeh^2,*,

Marziyeh Hajialyani¹

1Pharmaceutical Sciences Research Center, Faculty of Pharmacy, Kermanshah University of Medical Sciences, Kermanshah, Iran

2Research Center of Oils and Fats, Kermanshah University of Medical Sciences, Kermanshah, Iran

Journal of Reports in Pharmaceutical Sciences:Vol. 7, issue 3; 331-343

Published online:Aug 18, 2018

Article type:Research Article

Received:May 27, 2018

Accepted:Aug 08, 2018

How to Cite:Mahdi MojarrabAlireza PourasadollahHajar MotamedFarahnaz AhmadiLeila HosseinzadehMarziyeh Hajialyaniet al.Active Fractions of Dichloromethane Extract of Artemisia Aucheri Inhibit Proliferation of Human Breast Cancer MCF-7 Cells via Induction of Apoptosis.J Rep Pharm Sci.7(3):e147502.

Abstract

The antiproliferative effect of dichloromethane extract of Artemisia aucheri (A. aucheri) has been demonstrated previously on human cancerous cell lines. In the current study, further fractionation was carried out on the dichloromethane extract of A. aucheri and their cytotoxic effects were evaluated on three human cancer cell lines; SKNMC, MCF-7, and A2780. Cell viability was determined by MTT assay and activation of caspases was evaluated by spectrophotometry. Quantitative real time RT-PCR was used to evaluate the genes expression. Detection of DNA fragmentation was carried out by flow cytometry. The obtained results showed that fractions 5 and 7 (F5 and F7) have a potent cytotoxic effect, especially against MCF-7 cells. F5 and F7 also induced apoptosis through the DNA fragmentation and mitochondrial membrane potential (MMP) disruption in MCF-7 cells. The caspase-3, 9 enzyme activities were also increased after exposure to F5 and F7. Moreover, caspase-8 activity increased significantly after exposure to F7 but not F5. The level of mRNA expressions of Bax and Smac/DIABLO was increased after exposure to both fractions. A detectable decrease was also observed in the mRNA expression of Bcl-2 after exposure to F7. No change was observed in the level of mRNA expressions of tumor suppressor P53 after exposure to F7. Therefore, the cell cycle arrest and apoptosis induced by F7 could probably be mediated through a p53-independent mechanism. Taken together, these observations demonstrated that the cytotoxic effect of F5 and F7 on MCF-7 cells is likely exerted via apoptotic cell death.

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