Shao Yuming, Zhou Xuan, Zhou Shiqi, Long Junhui, Jin Linbo, Shi Xiaohua, Zhou Linxi, Zhang Yiming, Fan Dongli
Department of Plastic and Cosmetic Surgery, The Second Affiliated Hospital of Army Medical University, Chongqing 400038, China.
Department of Dermatology, Southwest Hospital Jiangbei Area (The 958th hospital of Chinese People's Liberation Army), Chongqing, China.
Colloids Surf B Biointerfaces. 2025 Apr;248:114488. doi: 10.1016/j.colsurfb.2024.114488. Epub 2024 Dec 30.
The chronic diabetic wounds represented by diabetes foot ulcers (DFUs) are a worldwide challenge. Excessive production of reactive oxygen species (ROS) and persistent inflammation caused by the impaired phenotype switch of macrophages from M1 to M2 during wound healing are the main culprits of non-healing diabetic wounds. Therefore, an injectable DMM/GelMA hydrogel as a promising wound dressing was designed to regulate the mitochondrial metabolism of macrophages via inhibiting succinate dehydrogenase (SDH) activity and to promote macrophage repolarization towards M2 type. DMM/GelMA hydrogel exhibited good biocompatibility, injectability and water absorption and retention capacity. In vitro studies showed that DMM/GelMA hydrogel inhibited SDH activity, recovered the decrease in mitochondrial membrane potential, and significantly reduced the production of ROS and inflammatory cytokines in the LPS-evoked macrophages. In vivo evaluations and RNA sequencing analysis demonstrated that DMM/GelMA hydrogel downregulated ROS generation, the ratio of M1/M2 macrophages and pro-inflammatory cytokine production in the full-thickness skin wound model in the diabetic mice. Additionally, DMM/GelMA hydrogel improved the wound-healing quality with thicker epidermis, more collagen deposition and higher ratio of collagen I/III by sustained release of DMM. These findings indicate this hydrogel has a great potential to be a biocompatible, injectable and anti-inflammatory dressing for better diabetic wound healing.
以糖尿病足溃疡(DFUs)为代表的慢性糖尿病伤口是一个全球性挑战。伤口愈合过程中巨噬细胞从M1型到M2型的表型转换受损,导致活性氧(ROS)过度产生和持续性炎症,这是非愈合性糖尿病伤口的主要原因。因此,设计了一种可注射的DMM/GelMA水凝胶作为一种有前景的伤口敷料,通过抑制琥珀酸脱氢酶(SDH)活性来调节巨噬细胞的线粒体代谢,并促进巨噬细胞向M2型再极化。DMM/GelMA水凝胶表现出良好的生物相容性、可注射性以及吸水和保水能力。体外研究表明,DMM/GelMA水凝胶抑制SDH活性,恢复线粒体膜电位的降低,并显著减少脂多糖诱导的巨噬细胞中ROS和炎性细胞因子的产生。体内评估和RNA测序分析表明,在糖尿病小鼠的全层皮肤伤口模型中,DMM/GelMA水凝胶下调了ROS生成、M1/M2巨噬细胞比例和促炎细胞因子的产生。此外,DMM/GelMA水凝胶通过持续释放DMM提高了伤口愈合质量,表现为表皮更厚、胶原沉积更多以及I/III型胶原比例更高。这些发现表明,这种水凝胶具有巨大的潜力,有望成为一种生物相容性好、可注射且具有抗炎作用的敷料,以促进更好的糖尿病伤口愈合。