Abstract
The treatment of chronic wound is an important topic of current clinical issue. Neovascularization plays a crucial role in skin wound healing by delivering fresh nutrients and oxygen to the wound area. The aim of this study was to investigate the mechanisms of urolithin A (UA) in angiogenesis during wound healing. The results of in vitro experiments showed that treatment with UA (5–20 μM) promoted the proliferation, migration, and angiogenic capacity of HUVECs. Furthermore, we investigated the effect of UA in vivo using a full-thickness skin wound model. Subsequently, we found that UA promoted the regeneration of new blood vessels, which is consistent with the results of accelerated angiogenesis in vitro experiments. After UA treatment, the blood vessels in the wound are rapidly formed, and the deposition and remodeling process of the collagen matrix is also accelerated, which ultimately promotes the effective wound healing. Mechanistic studies have shown that UA promotes angiogenesis by inhibiting the PI3K/AKT pathway. Our study provides evidence that UA can promote angiogenesis and skin regeneration in chronic wounds, especially ischemic wounds.
Highlights
Skin wounds remain a major global public health problem due to the increasing number of burns, trauma, and chronic diseases and can result in pain, infection, and even amputation (Valencia et al, 2001; Eberhardt and Raffetto, 2014)
We report that urolithin A (UA) has a therapeutic effect on the repair of rat skin wounds by accelerating angiogenesis
The mechanism of UA promoting wound healing may be related to the inhibition of the PI3K/AKT signaling pathway
Summary
Skin wounds remain a major global public health problem due to the increasing number of burns, trauma, and chronic diseases and can result in pain, infection, and even amputation (Valencia et al, 2001; Eberhardt and Raffetto, 2014). The new vessel and granulation tissue are destroyed, causing bleeding and secondary injury, which is unfavorable for wound healing and results in unbearable pain. Angiogenesis is a key factor in wound healing caused by chronic and ischemic injuries (Folkman, 1995). Endothelial cells are known to be key cells in angiogenesis, which are responsible for Urolithin A in Wound Healing many biological activities such as proliferation, adhesion, and transport from pre-existing blood vessels. Various growth factors have been shown to promote endothelial cell proliferation, migration, differentiation, and angiogenesis, such as the vascular endothelial cell growth factor (VEGF) and basic fibroblast growth factor (bFGF), which have been used in the treatment of ischemic diseases (Scharpfenecker et al, 2007; Bir et al, 2014). Finding an affordable, less complication-promoting drug that promotes angiogenesis in skin wounds may be a better alternative solution
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