Exosome-loaded tannic acid–thioctic acid hydrogel enhances wound healing in coagulation disorders
Yuesheng Tu, Weixin Zheng, Zichu Ding, Jie Xiang, Qing Yang, Yuchen Liu, Jue Cao, Yuling Shen, Zinan Tang, Shen Lin, Lei Fan, Yaowen Xu, Bin Chen
Abstract
Hemophilia poses distinct challenges to wound healing, primarily due to uncontrolled bleeding and delayed tissue repair. This study explored a novel tannic acid-thioctic acid (TATA) hydrogel, enriched with exosomes derived from bone marrow mesenchymal stem cells, as a therapeutic strategy for enhancing skin wound healing in a hemophilia model. The hydrogel exhibited robust hemostatic efficacy, potent antioxidant activity, and the capacity to modulate the inflammatory microenvironment. Both in vitro and in vivo assessments demonstrated significantly accelerated wound closure, increased collagen deposition, and pronounced angiogenesis in the TATA Hydrogel-Exosome(TATA Hydrogel-Exos) treatment group relative to controls. Rheological evaluations confirmed the self-healing properties and mechanical durability, of the hydrogel, underscoring its potential for sustained therapeutic application. Importantly, no significant systemic toxicity was observed, indicating favorable biocompatibility. These multifunctional TATA Hydrogel-Exos present a promising therapeutic avenue for hemophilia-related wounds by integrating hemostasis, inflammation regulation, and tissue regeneration. The functional groups, chemical bonds, and fabrication process of Hydrogel-Exos, and exosomes derived from BMSCs, along with their ability to modulate the inflammatory microenvironment, promote angiogenesis, and enhance skin wound repair following hemophilic skin injury. • TATA Hydrogel-Exos shows strong hemostatic effects, enhancing wound healing. • Promotes angiogenesis with increased CD31 and VEGF expression. • Biocompatible with no systemic toxicity, suited for long-term use. • Anti-Inflammatory, reducing iNOS, boosting IL-10, Arg-1. • Proven to reduce bleeding time and blood loss in hemophilia models.