This study aimed to restore the skin barrier function from atopic dermatitis (AD) via treatment with leucine-rich glioma inactivated 3 (LGI3) peptide. Male NC/Nga mice (7 weeks, 20 g) were randomly allocated into three groups (control, AD, and LGI3 group). After induction of AD skin lesions with Dermatophagoides farinae ointment, mice were treated with LGI3. The clinical score of AD was the highest and the dorsal skin thickness was the thickest in the AD group. In contrast, LGI3 treatment improved the clinical score and the dorsal skin thickness compared to the AD model. LGI3 treatment suppressed histopathological thickness of the epithelial cell layer of the dorsal skin. LGI3 treatment could indirectly reduce mast cell infiltration through restoring the barrier function of the skin. Additionally, the filaggrin expression was increased in immunohistochemical evaluation. In conclusion, the ameliorating effect and maintaining skin barrier homeostasis in the AD murine model treated with LGI3 could be attributed to complete re-epithelialization of keratinocytes. Hence, LGI3 might be considered as a new potential therapeutic target for restoring skin barrier function in AD.

中文翻译：

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亮氨酸丰富的神经胶质瘤灭活3（LGI3）肽对小鼠模型特应性皮炎受损的皮肤屏障功能的抑制作用。

这项研究旨在通过用富含亮氨酸的神经胶质瘤灭活3（LGI3）肽治疗来恢复特应性皮炎（AD）的皮肤屏障功能。将雄性NC / Nga小鼠（7周，20 g）随机分为三组（对照组，AD和LGI3组）。在用粉状皮肤癣菌诱发AD皮肤损伤后软膏，小鼠用LGI3治疗。在AD组中，AD的临床评分最高，而背侧皮肤厚度最厚。相反，与AD模型相比，LGI3治疗改善了临床评分和背侧皮肤厚度。LGI3处理抑制了背部皮肤上皮细胞层的组织病理学厚度。LGI3处理可通过恢复皮肤的屏障功能间接减少肥大细胞浸润。另外，在免疫组织化学评估中丝蛋白的表达增加。总之，在用LGI3处理的AD小鼠模型中，改善作用和维持皮肤屏障稳态可归因于角质形成细胞的完全上皮化。因此，