Study ofthe molecular mechanisms of delayed wound healing by using klothomice,which have phenotypessimilar to skin ulcerof aged humans.

本研究的目的是通过α-klotho-deficient （klotho -deficient, α-klotho-deficient）表型与老年人类相似的小鼠，分析衰老导致伤口延迟愈合的分子机制。采用克罗托米皮肤缺损创面模型，观察创面愈合时间、组织学及mRNA表达情况。与野生型（WT）小鼠相比，klotho小鼠表现出伤口愈合延迟和肉芽形成受损。逆转录聚合酶链反应（RT-PCR）分析显示，与WT小鼠相比，klotho小鼠皮肤创面损伤中白细胞介素(IL)-1β、IL-6和肿瘤坏死因子(TNF)-α mRNA表达增强，laminin-5表达降低。

The aim of this study was to analyze the molecular mechanisms of delayed wound healing with agingby using α-klotho-deficient (klotho) mice,which have phenotypessimilar to those of aged humans.Wound healing time, histology and mRNA expression were investigated using a skin defect wound model of klothomice. Theklotho mice showed delayed wound healingandimpairedgranulation formation compared to those in wild-type (WT) mice.The reverse transcript polymerase chain reaction (RT-PCR)analysis revealed enhancement of the mRNA expression of interleukin(IL)-1β, IL-6and tumor necrosis factor (TNF)-α, and depressionof laminin-5 in skin wound lesions of klotho mice compared to the levels in WT mice.