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. 2021 Mar 9;21:87. doi: 10.1186/s12906-021-03262-w

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 2 — The effects of AA on the viability of human lung cancer cells. H460 (a), H23 (b), and A549 (c) cells were treated with AA (0, 1.5625, 3.125, 6.25, 12.5, 25.0 and 50 μM) for 24 h. Cell survival was evaluated by MTT assay. The plots present the percentage of cell viability ± SEM from three independent experiments (n = 3). *, p < 0.05 vs nontreated cells. H460 (d), H23 (e) and A549 (f) cells were treated with AA (0–50 μM) for 24 h. Anti-apoptotic Bcl-2 and Mcl-1 and pro-apoptotic Bax were examined by Western blot assay. Blots were reprobed with anti-GAPDH antibodies to confirm equal loading. The protein levels were quantified and normalized to the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) level. The data are the mean ± SEM from three independent experiments (n = 3). *, p < 0.05 vs nontreated cells