Ferrous lactate enhances pressure ulcer healing and is associated with improved inflammatory, fibroblast, and angiogenic responses.

Pressure ulcers (PUs), also termed pressure injuries, are chronic inflammatory wounds associated with recurrent ischemia-reperfusion (I/R), impaired fibroblast repair, poor vascularization, and delayed extracellular matrix remodeling. We evaluated ferrous lactate in hypoxia/reoxygenation-injured human dermal fibroblasts (HDFs) and in a rabbit PU model generated by cyclic magnetic compression. In HDFs subjected to I/R-like stress, ferrous lactate increased viability, proliferation, and scratch migration, reduced TNF-α, IL-6, and IL-1β, and increased IL-10 and TGF-β. For in vivo treatment, ferrous lactate was delivered topically in sodium alginate vehicle and compared with untreated, vehicle, and commercial comparator groups. On day 14, wound closure reached 94.73 ± 2.49% in the 2 mM ferrous lactate group, compared with 44.80 ± 4.18% in untreated controls, 61.90 ± 1.29% in the vehicle group, and 71.50 ± 3.80% in the commercial comparator group. Wound closure in the 2 mM group was significantly greater than that in the commercial comparator group (P < 0.05). Ferrous lactate treatment was also associated with improved re-epithelialization, granulation tissue formation, collagen deposition, and Ki67-positive cell proliferation, together with increased VEGF expression and CD31-positive vascular staining. These findings provide preliminary preclinical evidence that topical ferrous lactate promotes pressure ulcer repair.