Thymosin beta 4 improves dermal burn wound healing via downregulation of receptor of advanced glycation end products in db/db mice

Abstract

BackgroundThe delay of dermal burn wound healing caused by vascular disorders is a critical problem for many diabetic patients. Thymosin β4 (Tβ4), identified by subtractive cloning of endothelial cells on plastic versus basement membrane substrates, has been found to promote angiogenesis and dermal wound repair in rats, aged mice, and db/db diabetic mice. However, previous studies involving the role of Tβ4 in wound repair were limited to mechanical damage and dermal impairment. Thus, this study aimed to evaluate the improvement of healing of burn wounds by Tβ4 in relation to advanced glycation end products (AGE), which are pathological factors in diabetes. MethodsWe adapted a dermal burn wound in vivo model in which the dorsal skin of db/db mice was exposed for 10s to 100°C heated water to produce a deep second-degree burn 10mm in diameter. Five mg/kg of Tβ4 was then injected intradermally near the burn wound twice a week for 2weeks. ResultsAfter treatment, Tβ4 improved wound healing markers such as wound closure, granulation, and vascularization. Interestingly, Tβ4 reduced levels of receptor of AGE (RAGE) during the wound healing period. ConclusionsTβ4 exerts effects to remedy burn wounds via downregulation of RAGE. General significanceOur results suggest the potential importance of Tβ4 as a new therapy for impaired burn wound healing that is associated with diabetes.