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. 2014 Jul 7;14:226. doi: 10.1186/1472-6882-14-226

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Copyright © 2014 Saleh et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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The growth inhibitory effect of AVO on HL-60 cells is mediated by apoptosis. (A) Cultured HL-60 cells were treated with varying concentration of AVO-b or AVO-l (0.0 to 2.0 μg/mL) an apoptosis was analyzed by a flow cytometer after staining with FITC-annexin-V and 7-AAD. The scattered blots showing the percentages of early and late apoptosis are indicated for one experiment. The graph represents the summary mean percentages of apoptosis (early and late apoptosis) of two independent experiments for each concentration of the oil. HL-60 cells were treated with 8.0 μM etoposide as a positive control. Statistical analysis showed that all samples are significantly different (p < 0.05), when compared to untreated controls. (B) Genomic DNA was extracted from HL-60 cells treated with the different concentrations of AVO-l or AVO-b, and applied to agarose gel electrophoresis. DNA fragmentation in the gel was visualized by UV light after staining with ethidium bromide. Mark, is a DNA ladder marker.