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. 2019 Jun 18;19:134. doi: 10.1186/s12906-019-2561-1

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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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Fig. 9 — Schematic diagram illustrating CG-induced apoptotic effects in A549 and NCI-H1299 NSCLC cell lines. CG stimulated death receptor (DR5 and Fas)- and adaptor (FADD)-mediated apoptotic signaling pathways, as well as caspase-8 processing, which resulted in cytochrome c release that was regulated by Bcl-2, Bid, and Bax. Subsequently, caspase-9 and caspase-3 were activated, followed by cleaved PARP, which led to apoptosis. Furthermore, CG stimulated tumor suppressor p53, and the cell cycle was suppressed by a reduction in cyclin factors. Moreover, CG induced ROS generation through the control of ROS scavengers, such as SOD2 in mitochondria, and catalase