Oxidative stress in the skin of a model of atopic dermatitis caused by skin barrier disfunction

2014 Fiscal Year Final Research Report

• Project/Area Number: 23791271
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Dermatology
• Research Institution: Kagawa University
• Principal Investigator: NAKAI Kozo 香川大学, 医学部附属病院, 助教 (40363204)
• Project Period (FY): 2011-04-28 – 2015-03-31
• Keywords: アトピー性皮膚炎 / 皮膚バリア機能 / フィラグリン / 酸化ストレス

Outline of Final Research Achievements

The deranged skin barrier function due to reduction of filaggrin expression in epidermis causes atopic dermatitis. We found that the expression of important skin barrier function factors is reduced in the skin of a mouse model of atopic dermatitis. N-acetylcysteine, an antioxidant, recovered the reduced expression of important skin barrier function factors. Moreover, topical application of N-acetylcysteine recovered the skin barrier function in human atopic dermatitis patients. These findings suggest that oxidative stress regulates the epidermal keratinization and skin barrier function.

Free Research Field

皮膚科学