The Suppressive Effect of Leucine-Rich Glioma Inactivated 3 (LGI3) Peptide on Impaired Skin Barrier Function in a Murine Model Atopic Dermatitis

Pharmaceutics

JoonSeok Bang¹  Dong-Seok Kim²  EonSub Park³  JongHyuk Lee⁴  JiHoon Jeong⁵  UiSeok Kim⁵  TaeWoo Jung⁵  JinWoo Park⁵  A.M. Abd El-Aty⁶ 

[1] College of Pharmacy, Sookmyung Women’s University, Seoul 04310, Korea;Department of Biochemistry, College of Medicine, Chung-Ang University, Seoul 06974, Korea;Department of Pathology, College of Medicine, Chung-Ang University, Seoul 06974, Korea;Department of Pharmaceutical Engineering, College of Life and Health Science, Hoseo University, Asan 31499, Korea;Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul 06974, Korea;Department of Pharmacology, Faculty of Veterinary Medicine, Cairo University, Giza 12211, Egypt;

关键词: atopic dermatitis;    leucine-rich glioma inactivated 3 (LGI3) peptide;    keratosis;    skin barrier;    filaggrin;   

DOI  :  10.3390/pharmaceutics12080750

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown