Abstract
Clinicians often experience delayed epithelialization in diabetic patients, for which a high glucose condition is one of the causes. However, the mechanisms underlying delayed wound closure have not been fully elucidated, and effective treatments to enhance epithelialization in patients with hyperglycaemia have not been established. Here we propose a new reagent, acylated homoserine lactone (AHL), to improve the delayed epithelialization due to the disordered formation of a basement membrane of epidermis in hyperglycaemic rats. Acute hyperglycaemia was induced by streptozotocin injection in this experiment. Full thickness wounds were created on the flanks of hyperglycaemic or control rats. Histochemical and immunohistochemical analyses were performed to identify hyperglycaemia-specific abnormalities in epidermal regeneration by comparison between groups. We then examined the effects of AHL on delayed epithelialization in hyperglycaemic rats. Histological analysis showed the significantly shorter epithelializing tissue (P < 0.05), abnormal structure of basement membrane (fragmentation and immaturity), and hypo- and hyperproliferation of basal keratinocytes in hyperglycaemic rats. Treating the wound with AHL resulted in the decreased abnormalities of basement membrane, normal distribution of proliferating epidermal keratinocytes, and significantly promoted epithelialization (P < 0.05) in hyperglycemic rats, suggesting the improving effects of AHL on abnormal epithelialization due to hyperglycemia.
Highlights
Delayed wound healing is one of the most important complications of diabetes mellitus
These results indicated that wound healing was delayed in hyperglycaemia
These results indicated that epithelialization was delayed under conditions of hyperglycaemia
Summary
Delayed wound healing is one of the most important complications of diabetes mellitus. The prolonged healing period of chronic ulcers substantially increases the risk of wound infection [1] and medical costs [2], and decreases the quality of life of diabetic patients [3]. Clinicians are increasingly experiencing diabetic patients with chronic wounds with little or no advance in wound closure or tylosis of the wound edge, despite using these approaches, suggesting that epithelialization is disrupted in diabetic patients [6]. Epithelialization is initiated by the migration of basal keratinocytes over the provisional wound matrix. Previous reports have revealed that high glucose conditions inhibit the migration and proliferation of normal human keratinocytes in vitro, suggesting that a high glucose condition is one of reasons for delayed wound closure in diabetes [11]
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