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

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.