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. 2020 Jul 6;20:209. doi: 10.1186/s12906-020-02965-w

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© The Author(s) 2020

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. 5 — Myricetin induced autophagy by inhibiting the activation of the PI3K/Akt/mTOR signalling pathway in HCT116 and SW620 cells. a LC3-I/II and Beclin-1 were detected by Western blotting with β-actin as the loading control. b Quantification of the Western blotting results with a histogram. c Transmission electron microscopy showed the number of autophagosomes (rectangle) in the cells treated with myricetin. d Protein levels were detected by Western blotting with β-actin as the loading control. Cells were treated with 50 or 100 μmol/L myricetin for 48 h. The Western blots were analysed by densitometry in ImageJ, and the myricetin treatment group was compared with the control group. The experiment was repeated three times (*p < 0.05, **p < 0.01, and ***p < 0.001 vs. control)