Shikonin hastens diabetic wound healing by inhibiting M1 macrophage polarisation through the MAPK signaling pathway.

Diabetes is an endocrine disorder characterized by abnormally elevated blood glucose levels. Diabetic patients often exhibit impaired wound healing capabilities, particularly in the lower limbs, which is one of the numerous complications of diabetes. This is a significant factor leading to recurrent inflammation, disability, and even amputation. The primary objective of this study is to explore the mechanism by which shikonin accelerates diabetic wound healing by modulating macrophage phenotypes, particularly its role in the MAPK signaling pathway. To this end, we used a diabetic rat model and analyzed the effects of shikonin on the wound healing process and macrophage polarization in both in vivo and in vitro experiments. Additionally, we used immunofluorescence staining and Western blot techniques to detect the expression levels of macrophage polarization markers and proteins related to the MAPK signaling pathway. The results verify that shikonin significantly accelerated wound healing in diabetic rats and inhibited the polarization of M1 macrophages, reducing the expression of pro-inflammatory factors, while promoting the polarization of M2 macrophages, increasing the expression of anti-inflammatory factors. This process was accompanied by the regulation of the MAPK signaling pathway, indicating that shikonin accelerates diabetic wound healing by regulating the MAPK signaling pathway to inhibit the inflammatory phenotype of macrophages, showing significant clinical application prospects.