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. 2023 Jan 19;28:5. doi: 10.1186/s11658-023-00417-0

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© The Author(s) 2023

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/.

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Fig. 9 — Schematic diagram showing the potential mechanism of PBM to promote SCI repair. At the cellular level, the expression of lncRNA TUG1 increased after the induction of M1 macrophages, which promoted the polarization and inflammatory response of M1 macrophages and aggravated neuronal damage. In mechanism, tug1 can promote TLR3 expression by adsorbing miR-1192, while PBM inhibits this pathway. PBM reduced the expression of TUG1, TLR3 and inflammatory cytokines in spinal cord tissue, and promoted the recovery of motor function