糖尿病脚部伤口中的细菌,通过破坏皮肤细胞来愈合伤口;分解其副产物可恢复恢复。 A bacterium in diabetic foot wounds blocks healing by damaging skin cells; breaking down its byproduct restores recovery.

新加坡和瑞士的科学家发现,糖尿病脚溃疡 -- -- Enterococcus faecalis -- -- 中的一种常见细菌通过损害皮肤细胞的代谢过程生产过氧化氢,从而损害伤口的愈合。 Scientists in Singapore and Switzerland have found that a common bacterium in diabetic foot ulcers, Enterococcus faecalis, impairs wound healing by producing hydrogen peroxide through a metabolic process that damages skin cells. 这会阻止细胞迁移到关闭伤口. This prevents cells from migrating to close wounds. 添加氧化物分解酶催化酶, 扭转了损伤, 恢复了愈合. Adding the enzyme catalase, which breaks down hydrogen peroxide, reversed the damage and restored healing. 这种方法避免抗生素,针对有害的副产品而不是杀死细菌,可能导致新的伤口包扎,以加快康复速度,减少感染,防止截肢。 The approach, which avoids antibiotics and targets harmful byproducts instead of killing bacteria, could lead to new wound dressings to speed recovery, reduce infections, and prevent amputations. 研究结果于2026年1月17日在《科学进步》上公布。 The findings were published in Science Advances on January 17, 2026.