PDF(Pubmed)
Abstract：
BACKGROUND: Diabetes mellitus (DM) presents impediment to wound healing. While ultraviolet B (UVB) exposure showed therapeutic potential in various skin conditions, its capacity to mediate diabetic wound healing remains unclear. To investigate the efficacy of UVB on wound healing and its underlying basis.
METHODS: Male C57BL/6 mice were subjected to the high-fat diet followed by streptozotocin administration to establish the diabetic model. Upon confirmation of diabetes, full-thickness wounds were inflicted and the treatment group received UVB radiation at 50 mJ/cm2 for 5 min every alternate day for 2 weeks. Wound healing rate was then assessed, accompanied by evaluations of blood glucose, lipid profiles, CD31 expression, and concentrations of ghrelin and leptin. Concurrently, in vitro studies were executed to evaluate the protective role of ghrelin on human umbilical vein endothelial cells (HUVEC) under high glucose (HG) conditions.
RESULTS: Post UVB exposure, there was a marked acceleration in wound healing in DM mice without alterations in hyperglycemia and lipid profiles. Compared to non-UVB-exposed mice, the UVB group showed enhanced angiogenesis manifested by a surge in CD31 expression. This trend appeared to be in harmony with the elevated ghrelin levels. In vitro experiments indicated that ghrelin significantly enhanced the migratory pace and angiogenic properties of HUVEC under HG-induced stress, potentially mediated by an upregulation in vascular endothelial growth factor expression.
CONCLUSIONS: UVB exposure bolstered wound healing in diabetic mice, plausibly mediated through augmented angiogenesis induced by ghrelin secretion. Such findings underscore the vast potential of UVB-induced ghrelin in therapeutic strategies targeting diabetic wound healing.
METHODS: Male C57BL/6 mice were subjected to the high-fat diet followed by streptozotocin administration to establish the diabetic model. Upon confirmation of diabetes, full-thickness wounds were inflicted and the treatment group received UVB radiation at 50 mJ/cm2 for 5 min every alternate day for 2 weeks. Wound healing rate was then assessed, accompanied by evaluations of blood glucose, lipid profiles, CD31 expression, and concentrations of ghrelin and leptin. Concurrently, in vitro studies were executed to evaluate the protective role of ghrelin on human umbilical vein endothelial cells (HUVEC) under high glucose (HG) conditions.
RESULTS: Post UVB exposure, there was a marked acceleration in wound healing in DM mice without alterations in hyperglycemia and lipid profiles. Compared to non-UVB-exposed mice, the UVB group showed enhanced angiogenesis manifested by a surge in CD31 expression. This trend appeared to be in harmony with the elevated ghrelin levels. In vitro experiments indicated that ghrelin significantly enhanced the migratory pace and angiogenic properties of HUVEC under HG-induced stress, potentially mediated by an upregulation in vascular endothelial growth factor expression.
CONCLUSIONS: UVB exposure bolstered wound healing in diabetic mice, plausibly mediated through augmented angiogenesis induced by ghrelin secretion. Such findings underscore the vast potential of UVB-induced ghrelin in therapeutic strategies targeting diabetic wound healing.
摘要：
背景：糖尿病（DM）阻碍伤口愈合。虽然紫外线B（UVB）暴露在各种皮肤状况下显示出治疗潜力，其介导糖尿病伤口愈合的能力尚不清楚.目的探讨UVB对创面愈合的影响及其基础。
方法：雄性C57BL/6小鼠高脂饮食后给予链脲佐菌素建立糖尿病模型。在确认糖尿病后，造成全层伤口，治疗组每天接受50mJ/cm2的UVB辐射5分钟，连续2周。然后评估伤口愈合率，伴随着对血糖的评估，脂质分布，CD31表达，以及生长素释放肽和瘦素的浓度。同时,在高糖（HG）条件下，进行了体外研究以评估ghrelin对人脐静脉内皮细胞（HUVEC）的保护作用。
结果：UVB暴露后，DM小鼠伤口愈合明显加速,高血糖和血脂谱没有改变.与非UVB暴露小鼠相比，UVB组血管生成增强,表现为CD31表达激增.这种趋势似乎与生长素释放肽水平的升高相一致。体外实验表明ghrelin能显著增强HG诱导应激下HUVEC的迁移速度和血管生成特性,可能由血管内皮生长因子表达上调介导。
结论：UVB暴露促进糖尿病小鼠伤口愈合，通过ghrelin分泌诱导的血管生成增强可能介导。这些发现强调了UVB诱导的ghrelin在针对糖尿病伤口愈合的治疗策略中的巨大潜力。
方法：雄性C57BL/6小鼠高脂饮食后给予链脲佐菌素建立糖尿病模型。在确认糖尿病后，造成全层伤口，治疗组每天接受50mJ/cm2的UVB辐射5分钟，连续2周。然后评估伤口愈合率，伴随着对血糖的评估，脂质分布，CD31表达，以及生长素释放肽和瘦素的浓度。同时,在高糖（HG）条件下，进行了体外研究以评估ghrelin对人脐静脉内皮细胞（HUVEC）的保护作用。
结果：UVB暴露后，DM小鼠伤口愈合明显加速,高血糖和血脂谱没有改变.与非UVB暴露小鼠相比，UVB组血管生成增强,表现为CD31表达激增.这种趋势似乎与生长素释放肽水平的升高相一致。体外实验表明ghrelin能显著增强HG诱导应激下HUVEC的迁移速度和血管生成特性,可能由血管内皮生长因子表达上调介导。
结论：UVB暴露促进糖尿病小鼠伤口愈合，通过ghrelin分泌诱导的血管生成增强可能介导。这些发现强调了UVB诱导的ghrelin在针对糖尿病伤口愈合的治疗策略中的巨大潜力。
