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

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Kim U. S., Park J. W., Park E. S., Bang J. S., Jung T. W., Kim D., ...Daha Fazla

PHARMACEUTICS, cilt.12, sa.8, 2020 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 12 Sayı: 8
  • Basım Tarihi: 2020
  • Doi Numarası: 10.3390/pharmaceutics12080750
  • Dergi Adı: PHARMACEUTICS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, EMBASE, Directory of Open Access Journals
  • Anahtar Kelimeler: atopic dermatitis, leucine-rich glioma inactivated 3 (LGI3) peptide, keratosis, skin barrier, filaggrin, FILAGGRIN, ECZEMA, COLONIZATION, MUTATIONS, CHILDREN, ASTHMA
  • Atatürk Üniversitesi Adresli: Evet

Özet

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 withDermatophagoides farinaeointment, 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.