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. 2021 Dec 7;21:1307. doi: 10.1186/s12885-021-09021-x

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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. 3 — Ivermectin mediates mitochondrial dysfunction of ESCC cells. A. Intracellular ROS levels were investigated by DCFH-DA fluorescence in ESCC cells treatment with indicated; B. The expression levels of Bax and Bcl-2 were determined by western blot analysis; C. The expression of caspase cascade (cleaved-caspase 9, cleaved-caspase 3, PARP, cleaved PARP) were analyzed by western blotting; D. Mitochondrial membrane potential was observed by fluorescence microscope at 200 × magnifications, Scale bar = 50 μm; E. ATP production of ESCC cells after treated with ivermectin was detected; F. The mitochondrial DNA copy number in ESCC cells treatment with invermectin was evaluated using qRT-PCR. ^*P < 0.05, ^**P < 0.01.