Zhong Shuyan, Bai Zan, Wu Juan, Wu Menglu, Zhang Ren-Jian-Zhi, Lai Rongguang, Zheng Xinnan, Shu Maoguo, Du Huicong
Department of Plastic, Cosmetic and Maxilofacial Surgery, the First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, 710061,Shaanxi,China
Curr Med Chem. 2025 Jul 28. doi: 10.2174/0109298673379670250703084615.
Wound healing is a complex and dynamic biological process involving overlapping phases such as inflammation, proliferation, and tissue remodeling. Chronic wounds, which fail to heal in a timely manner, pose significant challenges in clinical practice. Static magnetic fields (SMFs) have shown potential in wound healing, particularly in their anti-inflammatory effects and ability to promote cell proliferation. However, the precise mechanisms underlying their effects remain unclear.
This study aims to investigate the effects of SMFs on wound repair and to explore the molecular mechanisms involved, particularly the role of key signaling pathways.
A rabbit ear full-thickness wound model was used to evaluate the effects of SMFs (160 mT) on wound healing. Normal human dermal fibroblasts (NHDFs), normal human epidermal keratinocytes (NHEKs), and human umbilical vein endothelial cells (HUVECs) were cultured under SMF conditions to assess their proliferation, migration, and angiogenic activity. Tissue repair, angiogenesis, and cell proliferation were analyzed through histological and immunohistochemical methods. Transcriptome sequencing and Western blotting were performed to identify key pathways affected by SMFs.
SMFs significantly accelerated wound healing in the rabbit ear model, as demonstrated by enhanced re-epithelialization, granulation tissue formation, and angiogenesis. in vitro, SMFs promoted the proliferation and migration of fibroblasts and keratinocytes, as well as tube formation in endothelial cells. Transcriptome and protein analyses revealed that SMFs activated the PI3K/AKT/mTOR signaling pathway, which played a critical role in regulating cell proliferation and angiogenesis.
This study demonstrates that SMFs promote wound healing by enhancing angiogenesis and cell proliferation through activation of the PI3K/AKT/mTOR signaling pathway. These findings provide a theoretical foundation for the application of SMFs as a non-invasive therapeutic approach for clinical wound management.
伤口愈合是一个复杂且动态的生物学过程，涉及炎症、增殖和组织重塑等相互重叠的阶段。慢性伤口无法及时愈合，在临床实践中构成了重大挑战。静磁场已显示出在伤口愈合方面的潜力，特别是其抗炎作用和促进细胞增殖的能力。然而，其作用的精确机制仍不清楚。
本研究旨在探讨静磁场对伤口修复的影响，并探索其中涉及的分子机制，特别是关键信号通路的作用。
使用兔耳全层伤口模型评估静磁场（160 mT）对伤口愈合的影响。在静磁场条件下培养正常人皮肤成纤维细胞（NHDFs）、正常人表皮角质形成细胞（NHEKs）和人脐静脉内皮细胞（HUVECs），以评估它们的增殖、迁移和血管生成活性。通过组织学和免疫组织化学方法分析组织修复、血管生成和细胞增殖情况。进行转录组测序和蛋白质印迹分析以确定受静磁场影响的关键通路。
在兔耳模型中，静磁场显著加速了伤口愈合，表现为上皮再形成、肉芽组织形成和血管生成增强。在体外，静磁场促进了成纤维细胞和角质形成细胞的增殖与迁移，以及内皮细胞的管腔形成。转录组和蛋白质分析表明，静磁场激活了PI3K/AKT/mTOR信号通路，该通路在调节细胞增殖和血管生成中起关键作用。
本研究表明，静磁场通过激活PI3K/AKT/mTOR信号通路增强血管生成和细胞增殖，从而促进伤口愈合。这些发现为静磁场作为临床伤口管理的非侵入性治疗方法的应用提供了理论基础。
