Negative pressure wound therapy promotes wound healing by suppressing macrophage inflammation in diabetic ulcers.

Abstract

Aim: This work aims to explore the biological role of negative pressure wound therapy (NPWT) in the treatment of diabetic ulcer. Materials & methods: Full-thickness skin defects were created in diabetic (db/db) and non diabetic (db/m) mice to create wound models. The mice werereceived NPWT or rapamycin injection. Mouse macrophage cells (Raw264.7) were treated with lipopolysaccharide to induceinflammatory response, and thenreceived negative pressure treatment. We observed the wound healing of mice and examined gene and protein expression and CD68+ macrophage levels. Results: NPWT notably enhanced the wound closure ratio, and inhibited the LC3-II/LC3-I ratio and Beclin-1 expression in diabetes mellitus (DM) mice. NPWT decreased CD68+ macrophage levels in wound tissues of DM mice. The influence conferred by NPWT was abolished by rapamycin treatment. Negative pressure repressed the LC3-II/LC3-I ratio and the expression of Beclin-1, TNF-α, IL-6 and IL-1β in the Raw264.7 cells. Conclusion: NPWT promotes wound healing by suppressing autophagy and macrophage inflammation in DM.