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. 2021 May 31;19:162. doi: 10.1186/s12951-021-00909-1

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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. 10 — Loss of lc3b aggravated pulmonary oxidative stress induced by CuONPs. Wild type and lc3b^-/- mice were intratracheally instilled of vehicle or 5 mg/kg CuONPs, respectively, then the lung tissues of indicated groups were collected 3 days after treatment. A The mRNA expression levels of Nfe2l2, Hspa5, Hmox1 and Gclm in mice lung tissues in the indicated groups were determined by QPCR analysis. B The protein expression levels of NRF2, HMOX1, BIP and GCLM in mice lung tissues in the indicated groups were determined by western blot analysis. β-actin was served as internal control. C Quantification of the relative protein expression levels shown in (B) *indicates p < 0.05 compared with indicated group