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. 2023 Aug 1;14:1230174. doi: 10.3389/fphar.2023.1230174

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Copyright © 2023 Yan, Zhou, Meng, Zhou, Jia, Li, Cui, Yu, Tang, Li, Zhang, Wang, Hou and Yang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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SaB inhibited pathologic fibrosis at the cellular level via CD36. (A–D) After knocking down CD36, fibrosis-related molecules (COL 1, COL 3, FN, and α-SMA) were down-regulated at both mRNA and protein levels in synovial fibroblast, the effect of which was similar to that seen after SaB treatment. Besides, the healing and adhesion abilities of synovial fibroblast were also impaired in a manner comparable to SaB treatment. Scale bar: 50 µm. (E–H) Synovial fibroblasts secreted more fibrosis-related molecules and showed considerably greater capacity for healing and adhesion after being transfected with CD36 overexpression plasmid. When transfecting plasmid into synovial fibroblast cultured with SaB, the anti-fibrotic effect of which was partially reversed. Scale bar: 50 μm *p < 0.05; **p < 0.01; ***p < 0.001.