Related Experiment Video
Updated: Feb 25, 2026
Protocol to Create Chronic Wounds in Diabetic Mice
Published on: September 25, 2019
Mitochondria-Targeted Antioxidant SkQ1 Improves Dermal Wound Healing in Genetically Diabetic Mice
Ilya A Demyanenko1, Vlada V Zakharova2, Olga P Ilyinskaya1
1Faculty of Biology, Lomonosov Moscow State University, Leninskie Gory 1-12, Moscow 119234, Russia.
Abstract:
Oxidative stress is widely recognized as an important factor in the delayed wound healing in diabetes. However, the role of mitochondrial reactive oxygen species in this process is unknown. It was assumed that mitochondrial reactive oxygen species are involved in many wound-healing processes in both diabetic humans and animals. We have applied the mitochondria-targeted antioxidant 10-(6'-plastoquinonyl)decyltriphenylphosphonium (SkQ1) to explore the role of mitochondrial reactive oxygen species in the wound healing of genetically diabetic mice. Healing of full-thickness excisional dermal wounds in diabetic C57BL/KsJ-db-/db- mice was significantly enhanced after long-term (12 weeks) administration of SkQ1. SkQ1 accelerated wound closure and stimulated epithelization, granulation tissue formation, and vascularization. On the 7th day after wounding, SkQ1 treatment increased the number of α-smooth muscle actin-positive cells (myofibroblasts), reduced the number of neutrophils, and increased macrophage infiltration. SkQ1 lowered lipid peroxidation level but did not change the level of the circulatory IL-6 and TNF. SkQ1 pretreatment also stimulated cell migration in a scratch-wound assay in vitro under hyperglycemic condition. Thus, a mitochondria-targeted antioxidant normalized both inflammatory and regenerative phases of wound healing in diabetic mice. Our results pointed to nearly all the major steps of wound healing as the target of excessive mitochondrial reactive oxygen species production in type II diabetes.
Insights
Mitochondria-targeted antioxidant SkQ1 significantly improved wound healing in diabetic mice by enhancing tissue repair and normalizing inflammation. This suggests mitochondrial reactive oxygen species play a key role in delayed diabetic wound healing.
Area of Science:
- Biomedical Science
- Cell Biology
- Diabetology
Background:
- Oxidative stress and mitochondrial reactive oxygen species (ROS) are implicated in delayed wound healing in diabetes.
- The specific role of mitochondrial ROS in diabetic wound repair remains largely unexplored.
Purpose of the Study:
- To investigate the role of mitochondrial ROS in diabetic wound healing using a mitochondria-targeted antioxidant.
- To evaluate the therapeutic potential of SkQ1 in accelerating wound closure and improving tissue regeneration in diabetic mice.
Main Methods:
- Administration of SkQ1, a mitochondria-targeted antioxidant, to genetically diabetic mice (C57BL/KsJ-db-/db-) with full-thickness excisional dermal wounds.
- Assessment of wound healing parameters including closure rate, epithelization, granulation tissue formation, and vascularization.
- Analysis of cellular infiltration (myofibroblasts, neutrophils, macrophages), lipid peroxidation, and inflammatory cytokines (IL-6, TNF).
- In vitro scratch-wound assay under hyperglycemic conditions to assess cell migration.
Main Results:
- Long-term SkQ1 administration (12 weeks) significantly enhanced wound healing in diabetic mice.
- SkQ1 accelerated wound closure, epithelization, granulation tissue formation, and vascularization.
- Treatment modulated inflammatory cell infiltration, increased myofibroblasts, and reduced neutrophils while increasing macrophages.
- SkQ1 lowered lipid peroxidation levels and improved cell migration in vitro under hyperglycemia.
Conclusions:
- Mitochondria-targeted antioxidant SkQ1 effectively normalized both inflammatory and regenerative phases of wound healing in diabetic mice.
- Excessive mitochondrial ROS production significantly impairs major steps of wound healing in type II diabetes.
- SkQ1 demonstrates therapeutic potential for treating delayed wound healing in diabetic conditions.
