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. 2023 Jun 28;13:10485. doi: 10.1038/s41598-023-34060-8

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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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Amifostine (AMI) inhibits PI3K/Akt/mTOR signaling pathway in bleomycin (BLM)-induced pulmonary fibrosis. (a) The effect of AMI on p-PI3K, p-Akt, p-mTOR, PI3K, Akt, and mTOR protein expression in lung tissue was determined using Western blot analysis. (b) Western blot density analysis. Data are expressed as mean ± SD (n = 6). ^⁎⁎P < 0.01 versus the control group. ^##P < 0.01 and ^#P < 0.05 versus the model group. ^&&P < 0.01 versus the AMI 200-mg/kg group.