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. 2021 Dec 3;8:62. doi: 10.1186/s40779-021-00356-x

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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. 7 — Silencing of β-catenin aggravated downregulation of the occludin, claudin-1 and ZO-1 proteins, and reduced the proliferation and migration of RBMVECs following OGD/R. a Western blotting showed that Si1 was the most effective siRNA for silencing endogenous β-catenin gene expression. ^&P < 0.001, compared with the NC group; *P < 0.001, compared with the Si3 group; ^#P < 0.001, compared with the Si2 group. b Representative Western blotting images of occludin, claudin-1 and ZO-1 proteins in RBMVECs in each group. c Cell scratch test showed that proliferation and migration repair ability of RBMVECs in each group. All scale bars = 250 µm. Data are presented as the mean ± standard deviation (SD) from three independent experiments. *P < 0.001, compared with the normal group; ^#P < 0.001, compared with the control-siRNA group. NC group negative control group; OGD/R oxygen–glucose deprivation and reoxygenation; RBMVECs rat brain microvascular endothelial cells