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. 2017 Aug 30;7:10001. doi: 10.1038/s41598-017-10582-w

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© The Author(s) 2017

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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Peripheral serotonin regulated postoperative intra-abdominal adhesion formation in mice. After the surgery, serum serotonin was substantially released. Serotonin facilitated the following functions: recruitment of inflammatory cells and fibroblasts to the injury site, damage related to oxidative stress to the endotheliocyte, and the disorder of the fibrinolytic system, all of which resulted in collagen deposition, angiogenesis via the up-regulation of VEGF expression, and the secretion of extracellular matrix (ECM) via the up-regulation of TGF-β1 expression. The above mechanisms contributed to postoperative intra-abdominal adhesion formation.