Table 6 Investigations on melatonin and diabetic wound healing
From: Melatonin: new insights on its therapeutic properties in diabetic complications
| Type of study | Route of administration | Treatment duration | Targets | Effect(s) | Refs. | |
|---|---|---|---|---|---|---|
| In vivo dose (animal) | In vitro concentration (cell type) | |||||
| 1.2 mg/kg (male Sprague–Dawley rats) | – | Intra‐dermal | 1 week | iNOS, COX‐1, COX‐2, VEGF, arginase‐I, arginase‐II, HO‐1 and HO‐2 | Melatonin improved the quality of wound healing and scar formation | [190] |
| – | 10, 20, 50, 100, and 200 μM (endothelial progenitor cells (EPCs)) | – | 2 h | mTOR, 4EBP1, AMPKα, p70S6K, and P62 | Melatonin inhibited apoptosis and dysfunction of EPCs via autophagy flux stimulation | [191] |
| – (male ICR mice) | 1 μm Umbilical cord blood (UCB)‐MSCs | 24 h | FAK/paxillin, Cdc42/Arp2/3, PKC, Gαq and | – | Melatonin enhanced wound closure, granulation, and re‐epithelialization at mouse skin wound sites | [192] |
| – | 1 mM keratinocytes | 24 h | TNF-α, IL-1β, IL-6, IL-8, ROS, SOD, MDA | – | Melatonin increased migration and proliferation and reduced apoptosis of keratinocytes | [193] |