Abstract
Clinical studies indicate antibiotic bone cement with propeller flaps improves diabetic foot wound repair and reduces amputation rates, but the molecular mechanisms, particularly key proteins' role remain largely unexplored. This study assessed the efficacy of antibiotic bone cement for treating diabetic foot wounds, focusing on molecular impact on ROCK1. Sixty patients were randomized into experimental (EXP, n = 40) and control (CON, n = 20) groups, treated with antibiotic bone cement and negative pressure. Wound healing rate, amputation rate, wound secretion culture and C-reactive protein (CRP) changes, were monitored. Comprehensive molecular investigations were conducted and animal experiments were performed to further validate the findings. Statistical methods were employed to verify significant differences between the groups and treatment outcomes. The EXP group showed significant improvements in wound healing ( χ2<math> <semantics> <mrow><msup><mi>χ</mi> <mn>2</mn></msup> </mrow> <annotation>$$ {\chi}^2 $$</annotation></semantics> </math> = 11.265, p = 0.004) and reduced amputation rates. Elevated levels of ROCK1, fibroblasts and VGF were observed in the trauma tissue post-treatment in the experimental group compared to pre-treatment and the control group (all p < 0.05). Improved trauma secretion culture and CRP were also noted in the EXP group (all p < 0.05). The study suggests that antibiotic bone cement enhances diabetic foot wound healing, possibly via upregulation of ROCK1. Further research is needed to elucidate the underlying molecular mechanisms and broader clinical implications.