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. 2019 Feb 25;9:2721. doi: 10.1038/s41598-019-39179-1

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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(A1). Morphological assessment of control (A1 c; the cells are viable as inferred from the green fluorescence) and treated (A1, 1 complex 1; & A1, 2 complex 2) A549 lung cancer cells. (A2) The graph shows data on percentage of cells that are normal and those afflicted with apoptosis and necrosis in the control and 24 h treated groups. (A3) The effects of complexes 1 and 2 on the cell cycle progression in lung cancer A549 cells. (A4) The bar diagram displays higher percentage of cells in sub G₀ − G₁ and G₂-M phases after treatment of A549 cancer cells with complexes 1 and 2. The cell cycle distribution was analyzed using Dean-Jett-Fox software and depicted as the histogram. (A5) The vascular sprouting has been damaged (marked by arrows) on exposure to complexes 1 and 2 (10 μM) compared to control at 0 h (C, 1 and 2) after 6 h (C′, 1′ and 2′) of treatment. (A6) The different angiogenic parameters such as vessel length, vessel size and number of junctions decreased on exposure to complexes 1 and 2 compared to control. (Data are expressed in Mean ± SD).