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. 2019 Dec 27;9:19890. doi: 10.1038/s41598-019-56535-3

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© The Author(s) 2019

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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CXCR4 signaling pathway was involved in hBD3-mediated autophagy suppression. Intestinal epithelial cells IEC-6 and Caco2 were incubated with CXCR4 inhibitor AMD3100 (10 μM, 24 h), and further treated with rapamycin (200 nM for IEC-6 or 50 Nm for Caco2, 24 h) and hBD3 (5 μg/ml, 12 h) as indicated. The expression of p62, Beclin1, LC3, p-mTOR and p-AKT in each group was assessed by western blotting (A) the LC3II/LC3I ratio and relative expression of p-mTOR and p-AKT were analyzed (B) with total mTOR and AKT as a loading control. CXCR4 knockdown efficiency was monitored (C) and analyzed (D) in IEC-6 and Caco2, respectively. After being incubated with CXCR4 siRNA for 36 h and treated with rapamycin and hBD3 mentioned above, cells in each group were lysed and subjected to western blotting using antibodies against p62, Beclin1, LC3, p-mTOR and p-AKT. (E) The LC3II/LC3I ratio and relative expression of p-mTOR and p-AKT were also analyzed (F) with the same methods referred to above. Data was displayed as mean ± SD from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001, ^#p > 0.05.