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. 2024 Feb 13;22:148. doi: 10.1186/s12967-024-04913-5

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© The Author(s) 2024

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/. 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. 6 — | ROS mediates cell proliferation and the EMT phenotype induced by H. pylori in GC cells. A The protein levels of β-actin, Vimentin, and E-cadherin were detected in AGS cells treated with NAC (10 mmol/L) for different periods of time (0 h, 3 h, 6 h, 9 h, and 12 h). The data is representative of 3 independent experiments. B Western blot analysis of β-actin, Vimentin, and E-cadherin in AGS cells with control group, infection of wild-type H. pylori strain PMSS1 (MOI = 200) for 12 h, and combination treatment of wild-type H. pylori strain PMSS1 (MOI = 200) and NAC (10 mmol/L) for 12 h. The data is representative of 3 independent experiments. C, D The IHC scores were evaluated and statistically compared for expression of E-cadherin and vimentin. E, F Representative images of IHC staining for E-cadherin and vimentin in Balb/c mice gastric tissues with control group (n = 10), H. pylori strain SS1 group (n = 10), and combination of H. pylori strain SS1 and NAC group (n = 10). (Magnification 100 × , and 400 × ; bars = 5 μm). G The migration assays were conducted in AGS cells with control, H. pylori, and combination treatment of NAC (10 mmol/L) and H. pylori groups for 12 h, positively stained cells were counted and summarized in the statistical graph. The data is representative of 3 independent experiments. (magnification × 100). H The invasion assays were conducted in AGS cells with control, H. pylori, and combination treatment of NAC (10 mmol/L) and H. pylori groups for 12 h, positively stained cells were counted and summarized in the statistical graph. The data is representative of 3 independent experiments. (magnification × 100). *p < 0.05. I The wound healing assays were conducted in AGS cells with control, H. pylori, and combination treatment of NAC (10 mmol/L) and H. pylori groups for 12 h. The scratch width was captured at 0 and 48 h after the scratch, the relative wound closure area was summarized in the statistical graph. The data is representative of 3 independent experiments. (magnification × 100). *p < 0.05, **p < 0.01, ***p < 0.001