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. 2023 Apr 21;13:6528. doi: 10.1038/s41598-023-33848-y

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© The Author(s) 2023

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 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/.

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Impaired autophagic flux and activated HIF-1α/BNIP3 pathway are demonstrated in the liver of irinotecan (IR)-treated mice. (A) Western blot analysis of LC3-II, Beclin1 and p62 protein levels in liver tissue. (B) Densitometric quantification of LC3-II, Beclin1 and p62. (C) Effects of irinotecan on the formation of hepatic acidic vesicular organelles (orange) was examined by acridine orange (AO) staining. (D) Immunofluorescence was performed on liver sections using pimonidazole (green) to detect hypoxic regions, nuclei were stained with DAPI (blue). (E) Western blot analysis of HIF-1α and BNIP3 protein levels in liver tissue. (F) Densitometric quantification of HIF-1α and BNIP3. The blots were cut prior to hybridisation with indicated primary antibodies. Data are presented as mean ± SD (n = 6), *P < 0.05 and **P < 0.01 compared with normal control (NC) group.