Bacteria and excessive inflammation are two main factors causing non-healing wounds. However, current studies have mainly focused on the inhibition of bacteria survival for wound healing while ignoring the excessive inflammation induced by dead bacteria-released lipopolysaccharide (LPS) or peptidoglycan (PGN). Herein, a boron-trapping strategy has been proposed to prevent both infection and excessive inflammation by synthesizing a class of reactive metal boride nanoparticles (MB NPs). Our results show that the MB NPs are gradually hydrolyzed to generate boron dihydroxy groups and metal cations while generating a local alkaline microenvironment. This microenvironment greatly enhances boron dihydroxy groups to trap LPS or PGN through an esterification reaction, which not only enhances metal cation-induced bacterial death but also inhibits dead bacteria-induced excessive inflammation both in vitro and in vivo, finally accelerating wound healing. Taken together, this boron-trapping strategy provides an approach to the treatment of bacterial infection and the accompanying inflammation.

细菌和过度炎症是造成伤口不愈合的两个主要因素。然而，目前的研究主要集中在抑制细菌存活以促进伤口愈合，而忽略了死亡细菌释放的脂多糖（LPS）或肽聚糖（PGN）引起的过度炎症。在此，提出了一种硼捕获策略，通过合成一类活性金属硼化物纳米粒子 (MB NPs) 来预防感染和过度炎症。我们的结果表明，MB NPs 逐渐水解产生二羟基硼和金属阳离子，同时产生局部碱性微环境。这种微环境极大地增强了硼二羟基，通过酯化反应捕获 LPS 或 PGN，它不仅增强金属阳离子诱导的细菌死亡，而且抑制死细菌诱导的体外和体内过度炎症，最终加速伤口愈合。总之，这种硼捕获策略提供了一种治疗细菌感染和伴随炎症的方法。