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Updated: May 22, 2026

Protocol to Create Chronic Wounds in Diabetic Mice
Published on: September 25, 2019
Topical insulin application improves healing by regulating the wound inflammatory response
Xuelian Chen1, Yan Liu, Xiong Zhang
1Department of Burn and Plastic Surgery, ShangHai JiaoTong University, School of Medicine Affiliated Ruijin Hospital, Shanghai, China.
Insulin accelerates wound healing by enhancing macrophage function and infiltration. This study shows insulin regulates inflammatory responses, crucial for effective wound repair and healing.
Area of Science:
- Biomedical Science
- Wound Healing Research
- Immunology
Background:
- Inflammation is a critical initial phase of wound healing, involving endothelial changes and immune cell activity.
- The inflammatory response controls contamination and infection while initiating tissue repair.
- Macrophages play a central role in regulating inflammation during the healing process.
Purpose of the Study:
- To investigate the effect of insulin on wound inflammatory response, particularly macrophage function.
- To determine if insulin-regulated inflammation contributes to insulin-accelerated wound healing.
Main Methods:
- Utilized mouse excisional wound models and in vitro studies.
- Observed the impact of insulin on macrophage infiltration, resolution, and function.
- Investigated the role of monocyte chemotactic protein-1 (MCP-1) in insulin-mediated healing.
Main Results:
- Insulin treatment advanced macrophage infiltration and resolution in mouse wounds.
- Insulin correlated with increased expression of monocyte chemotactic protein-1 (MCP-1).
- Blocking MCP-1 impaired wound healing despite insulin treatment; in vitro studies confirmed insulin's facilitation of macrophage chemotaxis, phagocytosis, and mediator secretion.
Conclusions:
- Insulin acts as a potent wound healing accelerant.
- Insulin enhances wound healing by regulating the inflammatory response, specifically modulating macrophage quantity and function.
- Targeting macrophage activity represents a key mechanism in insulin-induced accelerated wound healing.
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