Mitochondria-Targeted Antioxidant SkQ1 Improves Dermal Wound Healing in Genetically Diabetic Mice
| Autor: | Vasily N. Manskikh, Olga P. Ilyinskaya, Roman A. Zinovkin, Artem V. Fedorov, Vlada V. Zakharova, Vladimir P. Skulachev, Boris V. Chernyak, E. N. Popova, Ilya A. Demyanenko, Tamara V. Vasilieva, Olga Yu. Pletjushkina |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Aging Antioxidant Article Subject Plastoquinone medicine.medical_treatment Pharmacology medicine.disease_cause Biochemistry Diabetes Mellitus Experimental Lipid peroxidation Mice 03 medical and health sciences chemistry.chemical_compound medicine Animals lcsh:QH573-671 Mice Knockout chemistry.chemical_classification Wound Healing Reactive oxygen species integumentary system 030102 biochemistry & molecular biology lcsh:Cytology business.industry Granulation tissue Cell migration Dermis Cell Biology General Medicine Mitochondria Oxidative Stress 030104 developmental biology medicine.anatomical_structure Diabetes Mellitus Type 2 chemistry Immunology Tumor necrosis factor alpha Wound healing business Oxidative stress Research Article |
| Zdroj: | Oxidative Medicine and Cellular Longevity Oxidative Medicine and Cellular Longevity, Vol 2017 (2017) |
| ISSN: | 1942-0994 1942-0900 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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