Infliximab accelerates wound healing in diabetic mice by aggravating macrophage polarization

Abstract

Delayed wound healing is one vital complication of diabetes mellitus (DM) that adversely impacts patient quality of life. Infliximab (INF), a monoclonal tumor necrosis factor α (TNF-α) antibody, has been investigated for its therapeutic potential across various diseases through displaying anti-inflammation ability. However, the regulatory mechanisms by which INF influences and correlates with delayed wound healing in DM remain unclear. In this study, we first induced diabetes in mice using streptozotocin (STZ) to establish a DM model, and then excision wounds were generated. We observed that wound closure was significantly retarded in DM mice, but this effect was reversed following INF treatment (5 mg/kg). Moreover, INF treatment attenuated the heightened inflammation observed in DM mice. Furthermore, we found that INF expedited the M2 phenotype polarization in DM mice. Mechanistically, INF was shown to delay activation of the nuclear factor kappa-B (NF-κB) pathway. To sum up, our findings demonstrate that in diabetic mice, INF facilitates wound healing by modulating macrophage polarization, and refrained the NF-κB pathway, supporting INF as a promising treatment approach for improving wound healing in diabetics.

Keywords

• infliximab
• wound healing
• macrophage polarization
• diabetes mellitus
• nf-κb pathway