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尿石素A在全层皮肤伤口模型中促进血管生成和组织再生。

Urolithin A Promotes Angiogenesis and Tissue Regeneration in a Full-Thickness Cutaneous Wound Model.

作者信息

Feng Zhen-Hua, Chen Jia, Yuan Pu-Tao, Ji Zhong-Yin, Tao Si-Yue, Zheng Lin, Wei Xiao-An, Zheng Ze-Yu, Zheng Bing-Jie, Chen Bin, Chen Jian, Zhao Feng-Dong

机构信息

Department of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.

Key Laboratory of Musculoskeletal System Degeneration and Regeneration Translational Research of Zhejiang Province, Hangzhou, China.

出版信息

Front Pharmacol. 2022 Mar 14;13:806284. doi: 10.3389/fphar.2022.806284. eCollection 2022.

DOI:10.3389/fphar.2022.806284
PMID:35359856
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8964070/
Abstract

The treatment of chronic wound is an important topic of current clinical issue. Neovascularization plays a crucial role in skin wound healing by delivering fresh nutrients and oxygen to the wound area. The aim of this study was to investigate the mechanisms of urolithin A (UA) in angiogenesis during wound healing. The results of experiments showed that treatment with UA (5-20 μM) promoted the proliferation, migration, and angiogenic capacity of HUVECs. Furthermore, we investigated the effect of UA using a full-thickness skin wound model. Subsequently, we found that UA promoted the regeneration of new blood vessels, which is consistent with the results of accelerated angiogenesis experiments. After UA treatment, the blood vessels in the wound are rapidly formed, and the deposition and remodeling process of the collagen matrix is also accelerated, which ultimately promotes the effective wound healing. Mechanistic studies have shown that UA promotes angiogenesis by inhibiting the PI3K/AKT pathway. Our study provides evidence that UA can promote angiogenesis and skin regeneration in chronic wounds, especially ischemic wounds.

摘要

慢性伤口的治疗是当前临床研究的一个重要课题。新血管生成在皮肤伤口愈合中起着关键作用，它通过向伤口区域输送新鲜的营养物质和氧气来促进愈合。本研究旨在探讨尿石素A（UA）在伤口愈合过程中促进血管生成的机制。实验结果表明，用5-20μM的UA处理可促进人脐静脉内皮细胞（HUVECs）的增殖、迁移和血管生成能力。此外，我们使用全层皮肤伤口模型研究了UA的作用。随后，我们发现UA促进了新血管的再生，这与加速血管生成实验的结果一致。UA处理后，伤口中的血管迅速形成，胶原蛋白基质的沉积和重塑过程也加速，最终促进了伤口的有效愈合。机制研究表明，UA通过抑制PI3K/AKT信号通路促进血管生成。我们的研究提供了证据，证明UA可以促进慢性伤口，特别是缺血性伤口的血管生成和皮肤再生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/426e/8964070/1c76386e60e3/fphar-13-806284-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/426e/8964070/da7ecb1291dd/fphar-13-806284-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/426e/8964070/4ae720e8c43b/fphar-13-806284-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/426e/8964070/768f980b054f/fphar-13-806284-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/426e/8964070/dc45771ca67a/fphar-13-806284-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/426e/8964070/55cf6d08aac0/fphar-13-806284-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/426e/8964070/1c76386e60e3/fphar-13-806284-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/426e/8964070/da7ecb1291dd/fphar-13-806284-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/426e/8964070/4ae720e8c43b/fphar-13-806284-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/426e/8964070/768f980b054f/fphar-13-806284-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/426e/8964070/dc45771ca67a/fphar-13-806284-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/426e/8964070/55cf6d08aac0/fphar-13-806284-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/426e/8964070/1c76386e60e3/fphar-13-806284-g006.jpg

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