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. 2022 Jun 16;20:90. doi: 10.1186/s12958-022-00951-0

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© The Author(s) 2022

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 — The expression of LC3 and Beclin-1 and the localization of LC3 in testicular tissue. The LC3 protein was localized mainly in the cytoplasm of spermatogenic cells at all levels, showing a brownish yellow colour. The LC3 protein level in NOA patients was elevated in comparison with the LC3 protein level in the control group. B-C LC3 (B) and Beclin-1 (C) gene expression levels in the NOA group were enhanced. D-E LC3 (D) and Beclin-1 (E) protein expression levels in the NOA group were higher than the levels in the control group. *Statistically significant difference compared with the control group (P < 0.05)